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Oliveira, Catarina Isabel Alves. "Aspetos Farmacológicos da Coenzima Q10". Master's thesis, [s.n.], 2012. http://hdl.handle.net/10284/3563.
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Trabalho apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências FarmacêuticasA Coenzima Q10 é um composto que existe no nosso organismo. Tem atividade antioxidante, produz ATP, é lipossolúvel, tem absorção lenta e uma circulação enterohepática. Depois de ser descoberta tem sido alvo de vários estudos clínicos com duas finalidades: evidenciar as variações dos seus níveis plasmáticos em alterações fisiológicas ou patológicas e demonstrar o seu benefício terapêutico. Este trabalho teve como objetivo realizar uma revisão bibliográfica de vários artigos científicos publicados num intervalo de tempo de 5 anos em linguas inglesa e portuguesa, divulgados no Pubmed, Medline, Science Direct, que descrevessem estudos clínicos em que a Coenzima Q10 é um possível elemento essencial no tratamento de diversas patologias. Evidenciou-se que a Coenzima Q10 tem vindo a ser estudada exaustivamente em determinadas patologias e que em vários estudos clínicos descritos demonstrou ter um papel terapêutico benéfico. No entanto, é relevante considerar a existência de mais investigações futuras para determinar de forma mais concreta e segura os benefícios da Coenzima Q10 para a saúde. Coenzyme Q10 is a compound that exists in our body. It has an antioxidant activity, it produces ATP, it is lipossoluble, it has a slow absorption and an enterohepatic recirculation. After its discovery it has been the target of various clinic studies with two purposes: to evidence the variations of its plasmatic levels in physiological or pathological changes and demonstrate therapeutic benefits. This work aimed to do a bibliographic review of various scientific articles published in a time interval of 5 years in English and Portuguese languages disclosed in Pubmed, Medline, Science Direct which clinic studies were described to determine the Coenzyme Q10 as the essential possible element in the treatment of the respective disease. It was revealed that the Coenzyme Q10 has been extensively studied in some diseases and that in various described clinic studies it was showed to have a beneficial therapeutic role. However, it is important to refer the meede of further investigations in order to better evaluate the role of Coenzyme Q10 to health.
2
Santos, Sónia Raquel Neiva. "Aspectos bioquímicos e moleculares da coenzima Q10". Master's thesis, Universidade de Aveiro, 2011. http://hdl.handle.net/10773/7981.
Texto completo da fonteResumo:
Mestrado em Biologia Molecular e CelularA ubiquinona (também chamada de Coenzima Q10, CoQ10) é uma benzoquinona presente em praticamente todas as células do organismo que participam dos processos de produção de ATP e é sintetisada na membrana interna da mitocondria. A principal fonte de CoQ10 é obtida por síntese endógena e uma pequena parte é adquirida através da dieta. A CoQ10 desempenha diversas funções biológicas nas células, entre as que se destacam a de transportador de electrões na cadeia respiratória mitocondrial e a participação no sistema anti-oxidante do organismo. Como tal, uma deficiência de ubiquinona pode causar efeitos nocivos importantes no organismo, uma vez que se veriam implicadas estas funções chave do metabolismo celular. A deficiência primária de CoQ10 (MIM 607426) é uma doença rara, de transmissão autossómica recessiva e com uma apresentação clínica muito variável, estando associada a quatro principais fenótipos clínicos: 1) encefalopatia caracterizada por mioglobinúria mas também com envolvimento do sistema nervoso central; (2) doença predominantemente encefalopática com ataxia e atrofia cerebelar; (3) miopatia isolada com RRFs e armazenamento lipídico; (4) doença multissistémica tipicamente infantil e encefalopatia; (5) nefropatia isolada ou associada a encefalopatia. Se as mutações encontradas, nestes doentes, estiverem localizadas nos genes envolvidos na biossíntese da CoQ10, então classifica-se estes síndromes como primários, se pelo contrário, as mutações estão presentes noutros genes, estamos perante a formas secundárias. O objectivo deste estudo é identificar e caracterizar sob o ponto de vista bioquímico e molecular as formas primárias com alteração da cadeia respiratória mitocondrial (CRM), patologia ainda não diagnosticada no nosso país. Inicialmente será implementado o doseamento da CoQ10 no músculo, plasma e eventualmente em fibroblastos por HPLC-reversa por detecção electroquímica. Nos doentes com os valores baixos de CoQ10, vai-se proceder ao estudo molecular dos genes envolvidos na biossíntese, em que já existem alterações descritas, no sentido de estabelecer uma relação fenótipo-genótipo. Os doentes vão ser seleccionados pelo diagnóstico clínico suspeito e/ou com alterações da CRM compatíveis com deficiência da ubiquinona. Este trabalho vai permitir a identificação das deficiências de CoQ10 que são de extrema importância visto serem as únicas Citopatias Mitocondriais potencialmente tratáveis. Para além disso, a identificação das mutações responsáveis por esta deficiência, vai permitir a possibilidade de diagnóstico pré-natal e implementação de terapêutica precoce.
The ubiquinone (also known as Coenzyme Q10, CoQ10) is a benzoquinone present in virtually all body cells that participate in production of ATP, and is synthesized in the inner membrane of mitochondria. The main source of CoQ10 is the endogenous synthesis and only a small part is acquired through the diet. CoQ10 has several biological functions in cells, among which stand out the electron carrier function in the mitochondrial respiratory chain and the participation in the body’s anti-oxidant system. Thus, a ubiquinone deficiency can cause significant adverse effects on the body, since key functions involved in cellular metabolism are affected. The primary deficiency of CoQ10 (MIM 607426) is a rare autosomal recessive disease with a highly variable clinical presentation, and which is associated with four major clinical phenotypes: (1) encephalomyopathy characterized by mioglobinúria and brain involvement; (2) predominantly encephalopathic illness with ataxia and cerebellar atrophy, (3) isolated myopathy with ragged-red fibers (RRF's); (4) typical infantile multisystemic disease with encephalopathy and (5) isolated nephropathy or associated with encephalopathy. If the mutations found in these patients are located in genes involved in the biosynthesis of CoQ10, these syndromes are classified as primary, on the contrary, if mutations are present in other genes, these are secondary forms. The aim of this study is to identify and characterize, from the point of view of biochemical and molecular changes, the primary forms of CoQ10 deficiency with mitochondrial respiratory chain (CRM) alterations, a disease not yet diagnosed in our country. Initially it will be implemented the determination of CoQ10 in muscle, plasma and possibly in fibroblasts by reverse HPLC-electrochemical detection. In patients with low levels of CoQ10, will be carried out the molecular study of the genes involved in biosynthesis, for which there are already changes described, to establish a phenotype-genotype relationship. Patients will be selected by the suspected clinical diagnosis and / or changes in CRM compatible with ubiquinone deficiency. The work will allow the identification of the deficiencies of CoQ10 which are extremely important because they are the only potentially treatable mitochondrial cytopathies. In addition, the identification of mutations responsible for this deficiency will allow the possibility of prenatal diagnosis and implementation of early treatment. i ÍNDICE
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Sanchez, Paulo José. "Avaliação do desempenho em equinos suplementado com coenzima Q10". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/10/10135/tde-08042015-113247/.
Texto completo da fonteResumo:
Com o objetivo de se investigar o efeito da suplementação de coenzima Q10 sobre o desempenho de equinos em treinamento aeróbio, foram utilizados dez equinos do sexo masculino, castrados, da raça Puro Sangue Árabe, com idade de 48±8,15 meses e peso 473±34,75 kg, divididos em grupo controle (GC) e grupo suplementado (GS). O experimento foi conduzido no Laboratório de Pesquisa em Alimentação e Fisiologia do Exercício de Equinos (LABEQUI), pertencente à FMVZ-USP, no Campus Administrativo de Pirassununga, São Paulo, adotando-se o consumo diário individual de 2% do peso corpóreo, com base na matéria seca, sendo 50% de volumoso composto por feno de gramínea e 50% de concentrado comercial. Os animais inseridos no grupo suplementado (GS) receberam individualmente a inclusão diária de 800mg de coenzima Q10 adicionado à dieta de concentrado durante os 90 dias de experimento. Todos os animais foram exercitados cinco vezes por semana, durante sessenta minutos, na velocidade máxima de 15 km/h, em exercitador circular mecânico para cavalos, controlado eletronicamente. Durante o experimento foram realizados análise hematológica e bioquímica (AST, CK e LDH), mensuração da curva de glicose e de lactato, monitoramento da frequência cardíaca e sudorese dos equinos. Foi utilizado o delineamento inteiramente casualizado com medidas repetidas no tempo, com dados estatisticamente significantes sendo submetidos à análise de regressão. Através das análises hematológicas, bioquímicas, da curva glicose e de lactato, pode-se observar a higidez e a adaptação dos animais frente ao protocolo de treinamento. O grupo suplementado apresentou efeito de tratamento para a enzima creatinaquinase, e apresentou menor oscilação da frequência cardíaca e da taxa de sudação. Conclui-se que a suplementação de equinos atletas com coenzima Q10 submetidos a exercício aeróbio influenciou no desempenho atlético dos cavalosWith the goal of investigating the effect of Coenzyme Q10 supplementation on the performance of equines subject to aerobic exercise, ten pure Arabian geldings, aged 48±8,15 months and weighing 473±34,75 kg were divided into control group (GC) and supplemented group (GS). The experiment was performed at LABEQUI - Equine Nutrition and Exercise Physiology Research Laboratory, which belongs to FMVZ - USP, School of Veterinary Medicine and Animal Science of USP (São Paulo University), which belongs to Campus Pirassununga. Individual intake of food was considered 2% of body weight, of which 50% corresponded to grass hay and 50% to commercial pelleted concentrate. The horses in the supplemented group (GS) received a daily inclusion of 800 mg of coenzyme Q10, added to the concentrated food during the 80 days of the experiment. All animals were exercised five days per week, during sixty minutes, at a top speed of 15 km/h, in a electronically controlled circular mechanical walker. During the experiment, blood tests and biochemical analysis (AST, CK, and LDH) were conducted, as well as measurements of glucose and lactate curves and monitoring of heart frequency and perspiration. The method used was totally casual lineation with measures repeated in time, with statistically significant data being submitted to regression analysis. Animals’ healthiness and adaptation to the training protocol could be observed through hematological and biochemical analysis and glycemic and lactate curves. The supplemented group showed a treatment effect for the enzyme creatinekinase, and showed less fluctuation in heart rate and sweating rate.. It was concluded that supplementation with coenzyme Q10 of equine athletes submitted to aerobic exercise had a positive effect on the athletic performance of the horses
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Machado, Carla da Silva. "Possíveis efeitos citoprotetores do antioxidante da dieta coenzima Q10 em modelo de células neuronais". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-24102011-143836/.
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A coenzima Q10 é uma provitamina lipossolúvel sintetizada endogenamente e naturalmente encontrada em alimentos como a carne vermelha, peixes, cereais, brócolis e espinafre. É comercializada como suplemento alimentar e utilizada em formulações cosméticas. Localiza-se na membrana de organelas celulares como retículo endoplasmático, vesículas e membrana interna da mitocôndria, onde atua como um cofator essencial na cadeia respiratória. Apresenta propriedades antioxidantes e potencial no tratamento de doenças neurodegenerativas e neuromusculares. O objetivo deste trabalho foi investigar os possíveis efeitos protetores de uma formulação hidrossolúvel de coenzima Q10 em células PC12 expostas à cisplatina, um fármaco antineoplásico que tem a neurotoxicidade como um dos fatores limitantes à sua utilização. A linhagem celular PC12 (feocromocitoma de ratos) utilizada nesta investigação é um reconhecido modelo in vitro para estudos neuronais. Os métodos empregados foram os ensaios do MTT, cometa, citoma micronúcleo com bloqueio da citocinese, crescimento de neuritos e análise da expressão do gene Tp53. Os resultados obtidos na avaliação da citotoxicidade da coenzima Q10 (0,1 - 20 µg/mL) mostraram que este antioxidante foi citotóxico às células PC12 na concentração de 20,0 µg/mL e não apresentou citotoxicidade em baixas concentrações. Para os ensaios do citoma e cometa, foram selecionadas três concentrações não citotóxicas de coenzima Q10 (0,1; 0,5 e 1,0 µg/mL) que não apresentaram mutagenicidade e genotoxicidade às células PC12. O efeito protetor da coenzima Q10 sobre a cisplatina no ensaio do citoma foi caracterizado pela diminuição da freqüência de micronúcleos e brotos nucleares, entretanto a proteção da coenzima Q10 não foi evidenciada no ensaio cometa. Alterações significativas na expressão do gene Tp53 não foram observadas no tratamento coenzima Q10 (1,0 µg/mL) associado à cisplatina (0,1 µg/mL). A coenzima Q10 (0,1 e 1,0 µg/mL) não foi neurotóxica em células PC12 indiferenciadas e diferenciadas após exposição ao fator de crescimento do nervo, e seu melhor efeito neuroprotetor foi observado na menor concentração avaliada. A coenzima Q10 reduziu a citotoxicidade da cisplatina (10,0 µg/mL) em células PC12 indiferenciadas e estimulou o crescimento de neuritos em células PC12 diferenciadas. A determinação dos efeitos citoprotetores da coenzima Q10 em um modelo neuronal é importante para elucidar possíveis estratégias de neuroproteção que poderiam ser aplicadas aos pacientes submetidos à quimioterapia.Coenzyme Q10 is a liposoluble provitamin endogenously synthesized and naturally found in various foods items, such as meat, fish, cereals, broccoli and spinach. It is a dietary supplement in some countries and used in cosmetic formulations. Coenzyme Q10 is located in the membrane of cellular organelles such as endoplasmic reticulum, vesicles and inner mitochondrial membrane, where acts as an essential cofactor in the respiratory chain. It has antioxidant properties and potential in the treatment of neurodegenerative and neuromuscular diseases. The objective of this study was to investigate the possible protective effects of a water-soluble formulation of coenzyme Q10 in PC12 cells exposed to cisplatin, an anticancer drug that has neurotoxicity as a dose-limiting factor. The PC12 cell line (rat pheocromocytoma) used in this investigation is a recognized in vitro model for neuronal studies. The methods used were the MTT, comet, cytokinesis-block micronucleus cytome, neurite outgrowth assays and expression of Tp53 gene. The results obtained in the cytotoxicity of coenzyme Q10 (0.1-20 µg/mL) showed that this antioxidant was cytotoxic to PC12 cell at a concentration of 20.0 µg/mL and it was not cytotoxic at low concentrations. For the cytome and comet assays, were selected three non-cytotoxic concentrations of coenzyme Q10 (0.1, 0.5 and 1.0 µg/mL) without mutagenicity and genotoxicity PC12 cells. The protective effect of coenzyme Q10 in cytome assay was characterized by decreased frequency of micronuclei and nuclear buds induced by cisplatin, however the protection of coenzyme Q10 was not evidenced by the comet assay. No significant change in the Tp53 gene expression were observed in the coenzyme Q10 (1.0 µg/mL) plus cisplatin (0.1 µg/mL) treatment. Coenzyme Q10 (0.1 and 1.0 µg/mL) was not neurotoxic in undifferentiated and nerve growth factor differentiated PC12 cells and the lowest concentration evaluated showed the best neuroprotective effect. The coenzyme Q10 treatment reduced the citotoxicity of cisplatin (10.0 µg/mL) in undifferentiated PC12 cells and stimulated the neurite outgrowth in differentiated PC12 cells. Determination of the cytoprotective effects of the coenzyme Q10 in a neuronal model is important to elucidate possible strategies for neuroprotection that could be applied to patients undergoing chemotherapy.
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CASCELLA, Vincenza. "STUDIO DEL DANNO UDITIVO CAUSATO DA RUMORE O DA CISPLATINO: EFFETTO PROTETTIVO DI ACUVAL400 ED N-QTER". Doctoral thesis, Università degli studi di Ferrara, 2012. http://hdl.handle.net/11392/2389263.
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Hearing is one of the key functions in communication, making us capable to develop our ability to
interact with others.
The partial or total loss of this function leads to deafness causing significant social problems.
Hearing impairment is called hypoacusis and is one of the most common pathologies in our
society. Its prevalence varies from about 0.2% in children under 5 years of age to more than 40%
in adults over 75 years.
Several factors are responsible for hearing loss through oxidative stress, the process by which the
cochlear hair cells and neuronal cells of spiral ganglion go toward apoptosis or necrosis
(sensorineural hypoacusis).
Recently, there have been elucidated many aspects of mechanical and metabolic damage induced
by noise (noise-induced hearing loss, NIHL) and by treatment with a potent chemotherapy drug,
cisplatin (CDDP).
The ototoxicity induced by noise exposure and use of CDDP is characterised by sensory hair cell
death subsequent to overproduction of reactive oxygen species (ROS) (super-oxide anion,
hydrogen peroxide, hydroxyl radicals), responsible of lipid peroxidation, protein and DNA
damage.
In particular, the accumulation of ROS determines an increment or a modulation of the activity of
endogenous antioxidant enzymes such as glutathione (GSH) and superoxide dismutase (SOD).
Several studies report that by increasing the levels of antioxidants (for example through the use of
drugs or genetic manipulation) it is possible to promote survival of sensory hair cells and to protect
them from acoustic trauma and ototoxic agents.
Various papers report the use of different antioxidants (vitamins A, C, E, polyphenols, flavonoids
and organosulfur compounds) to treat either noise- or CDDP-induced hearing loss, due to their
ability to reduce oxidative stress.
Recent studies show how coenzyme Q10 (CoQ10), or ubiquinone, besides being an electron carrier
in the complexes I, II and III of the mitochondrial respiratory chain, is an ubiquitous scavenger of
free radicals, capable of preventing cochlear lipid peroxidation caused by acoustic trauma and
treatment with CDDP.
CoQ10 is particularly liposoluble therefore very difficult to be absorbed, so recently it has been
developed in a new soluble form, terclatrate CoQ10 (n-QTER).
Fetoni et al. used n-QTER and discovered that it could protect sensory cells from apoptosis.
Conklin et al. demonstrated how the CoQ10 is able to suppress the lipid-peroxidation, because it is
able to increase GSH and SOD levels. Based on the antioxidant properties of CoQ10, we hypothesized that this molecule may protect the
cochlea from acoustic trauma and from ototoxicity of CDDP.
In particular, it was evaluated the effect of an antioxidant dietary supplement, ACUVAL ® 400,
which contains n-QTER (0.32 mg) and an extract of Ginkgo biloba (Ginkgoselect ®), both known
for their functions of radical scavenging as well as many other healing properties.
From the data analysis obtained by administering different concentrations of n-QTER at different
times, before and after the damage induced by noise and by CDDP, it was found that in both cases
the protective effect was achieved with an additional dose of n-QTER (500 mg/ kg) in the ACUVAL
® 400 (100 mg/kg).
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RAMALHO, Flávia Camila Siqueira Pereira. "Efeito da coenzima Q10 no meio de fertilização in vitro de embriões bovinos". Universidade Federal Rural de Pernambuco, 2015. http://www.tede2.ufrpe.br:8080/tede2/handle/tede2/6251.
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In vitro embryo production (IVP) in cattle became an important commercial tool in genetic improvement programs of the world herd, being widely used for this purpose. However in vitro fertilization (IVF) can cause generation of reactive oxygen species that can affect embryo viability. Coenzyme Q10, an important cofactor in the transport chain of mitochondria has antioxidant function on lipid membrane and it was proved a direct correlation between the presence of Coenzyme Q10 and normal spermatozoa parameters such as density, motility, morphology and volume. The objective of this study was to evaluate the effect of Coenzyme Q10 on sperm function in IVF using conventional or sexed semen; also if the addition of this cofactor can improve embryo IVP in bovine oocytes. In experiment 1 was evaluated the effect of sperm function during incubation periods of sexed and conventional semen samples. In experiment 2, IVF medium was supplemented with 0 (control group), 5 μM, 10 μM, 20 μM of Coenzyme Q10. Bovine oocytes were collected from a slaughterhouse located 20 minutes from the lab. It was observed a negative effect of Coenzyme with significant differences in the rates of cleavage or in the production of blastocyst (p< 0.05) at a concentration of 20 μM when compared with all other groups with either sexed as conventional semen. These results demonstrate that supplementation of the Coenzyme Q10 in the IVF medium, do not alter spermatozoa function. We can also infer that there is a tendency to improve embryo production in the concentration of 5 μM in IVF medium.
A produção de embriões in vitro (PIV) em bovinos tornou-se importante ferramenta comercial nos programas de melhoramento genético do rebanho mundial como técnica de multiplicação, sendo amplamente utilizada para esse fim. Entretanto a Fertilização in vitro (FIV) provoca geração de espécies reativas de oxigênio que podem afetar a viabilidade embrionária. A Coenzima Q10, um cofator de importância na cadeia de transporte das mitocôndrias tem função antioxidante na membrana lipídica e foi verificado uma correlação direta entre a Coenzima e os parâmetros normais de sêmen tais como, densidade, motilidade, morfologia e o volume. O objetivo desse trabalho foi avaliar o efeito da Coenzima Q10 na função espermática em FIV utilizando-se sêmen convencional e sexado; e se a adição desse cofator pode melhorar a produção embrionária in vitro de oócitos bovinos. No Experimento o meio de FIV foi suplementado com 0 (grupo controle), 5 μM, 10 μM, 20 μM da Coenzima Q10. Os Oócitos foram coletados de um abatedouro localizado a 20 minutos do laboratório. Foi observado um efeito deletério da coenzima com diferença significativa nas taxas de clivagem ou na produção de blastocisto (p<0,05) na concentração de 20 μM quando comparado com os demais grupos tanto com sêmen sexado como convencional. Estes resultados demonstram que a suplementação da Coenzima Q10 no meio FIV não altera a função espermática, entretanto tem um efeito deletério a partir da concentração de 20 μM. Podemos ainda inferir que na concentração de 5 μM no meio FIV há uma tendência na melhoria da produção embrionária.
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Carnevali, Paola. "Effetti della somministrazione del Coenzima Q10 sullo stress ossidativo nella Sindrome di Down". Doctoral thesis, Università Politecnica delle Marche, 2007. http://hdl.handle.net/11566/242644.
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Carneiro, João Alexandre Matos [UNESP]. "Da coenzima Q10 sobre a viabilidade espermática de garanhões resistentes ou sensíveis à congelação". Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/151226.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Entre as vantagens da criopreservação seminal, destacam-se a otimização do uso de garanhões com comprovada superioridade genética, pela possibilidade do armazenamento de sêmen mesmo fora da estação de monta e a quebra das barreiras geográficas, que torna possível a remessa deste material para qualquer parte do mundo. Contudo, o processo de congelação de sêmen causa danos à célula espermática, sendo a peroxidação lipídica e o estresse oxidativo, ocasionada pela produção anormal de espécies reativas de oxigênio (EROs), as principais injúrias. Desta maneira, para se obter uma melhor qualidade seminal após a descongelação, é necessário adicionar aos diluentes seminais elementos que desempenhem função antioxidante, visando conter o aumento dos níveis dos agentes oxidantes. Coenzima Q10 (CoQ10) é um agente lipossolúvel promotor de energia, tendo como principal função transportar prótons e elétrons no processo de síntese de ATP na membrana mitocondrial interna, através da cadeia de transporte de elétrons. Ainda, a CoQ10 atua como um potente antioxidante em diversos sistemas biológicos, tais como, lipoproteínas e membranas, protegendo-os contra a oxidação, inibindo a formação de hidroperóxidos e, consequentemente, prevenindo a peroxidação lipídica. Desta forma, o objetivo deste estudo foi avaliar a ação da coenzima Q10 (CoQ10) no espermatozoide de garanhões resistentes (RC) e sensíveis (SC) a congelação. Cada ejaculado (n=24) foi dividido em nove tratamentos e submetido à congelação, sendo a CoQ10 adicionada ao diluente de centrifugação, nas concentrações de 25 μmol/L (CE25), 50 μmol/L (CE50), 75 μmol/L (CE75) e 100 μmol/L (CE100), ou ao de congelação nas mesmas concentrações, 25 μmol/L (FE25), 50 μmol/L (FE50), 75 μmol/L (FE75) e 100 μmol/L (FE100). No grupo controle não houve adição da CoQ10 em nenhum dos meios diluentes. O processo de descongelação foi realizado à 37ºC/30 segundos (T0) e, para avaliação após estresse térmico, 37ºC/30minutos (T30). Posteriormente, as células espermáticas foram avaliadas quanto a cinética, integridade da membrana plasmática (IMP), desestabilização da membrana (NCAP), produção de espécies reativas ao oxigênio (H2O2 e O2 -), atividade mitocondrial e peroxidação lipídica. De acordo com os resultados, não houve diferença significativa entre os grupos, tanto no momento T0 quanto no momento T30, para os garanhões classificados como RC (p>0,05), com exceção da peroxidação lipídica, que em ambos os momentos, os grupos tratados apresentaram valores menores quando comparados ao controle (p<0,05). Já para os animais classificados como SC, houve uma superioridade das células espermáticas tratadas com a CoQ10 (p<0,05), com exceção da concentração de O2 - e potencial mitocondrial no T0, em que não apresentaram diferença entre os grupos (p>0,05). As células espermáticas do grupo CE75 se mostraram superiores aos parâmetros avaliados em relação aos demais grupos. Podemos concluir que a CoQ10 promove uma diminuição do estresse oxidativo e maior viabilidade ao espermatozoide de garanhões sensíveis ao processo de congelação espermática.
Among the advantages of seminal cryopreservation, the optimization of using stallions with proven genetic superiority, the possibility of storing semen even outside the breeding season and the breaking of geographical barriers, which makes it possible to send this material to any part of the world can de highlighted. However, the process of semen freezing causes damage to the sperm cell, and the abnormal production of reactive oxygen species is caused by lipid peroxidation of the sperm membrane, which is a major cause of such injury. Thus, in order to obtain a better seminal quality after thawing, it is necessary to add to the diluents substances that play an antioxidant function, limiting levels of the oxidizing agents increase. Coenzyme Q10 is a liposoluble energy-promoting agent, whose main function is to transport protons and electrons in the process of ATP synthesis in the internal mitochondrial membrane, through the electron transport chain. Furthermore, CoQ10 (ubiquinol) acts as a potent antioxidant in several biological systems, such as lipoproteins and membranes, protecting them against oxidation, inhibiting the hydroperoxides formation and, consequently, preventing lipid peroxidation. In this way, the objective of this study was to discuss how CoQ10 may help reducing the oxidative stress caused by seminal cryopreservation process. This form, the objective of this study was to evaluate the antioxidant action of coenzyme Q10 (CoQ10) on spermatozoa from good freezers (GF) and bad freezers (BF) stallions. Each ejaculate (n=15) was divided into nine treatments and subject to freezing process. The CoQ10 was added to centrifugation extender at concentrations 25 μmols/L (CE25), 50 μmols/L (CE50), 75 μmols/L (CE75) and 100 μmols/L (CE100), or at the freezer extender at the same concentrations, 25 μmols/L (FE25), 50 μmols/L (FE50), 75 μmols/L (FE75) and 100 μmols/L (FE100). In the control group there was no addition of CoQ10 in any of the extenders. The thawing process was performed at 37ºC/30 seconds (T0) and at 37ºC/30 minutes (T30). Posteriorly, sperm cells were evaluated for kinetics, plasma membrane integrity (PMI), membrane desestabilization (NCAP), reactive oxygen species production (H2O2 and O2 -), mitochondrial activity and lipid peroxidation. According to the results, there was no significant difference between the groups, as well T0 moment as T30 moment, for good freezer stallions (p>0.05). However for bad freezer stallions, there was a superiority of the sperm cells that came into contact with CoQ10 (p <0.05), except for the O2 - concentration and mitochondrial potential (T0) in which there was no significant difference between the Groups (p> 0.05). The sperm cells of the CE75 group were superior in the evaluated parameters in relation to the other groups. We can conclude that CoQ10 promotes a reduction of oxidative stress and greater viability to the spermatozoa from bad freezer stallions at the freezing process.
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Carneiro, João Alexandre Matos. "Da coenzima Q10 sobre a viabilidade espermática de garanhões resistentes ou sensíveis à congelação". Botucatu, 2017. http://hdl.handle.net/11449/151226.
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Orientador: José Antonio Dell'Aqua JuniorResumo: Entre as vantagens da criopreservação seminal, destacam-se a otimização do uso de garanhões com comprovada superioridade genética, pela possibilidade do armazenamento de sêmen mesmo fora da estação de monta e a quebra das barreiras geográficas, que torna possível a remessa deste material para qualquer parte do mundo. Contudo, o processo de congelação de sêmen causa danos à célula espermática, sendo a peroxidação lipídica e o estresse oxidativo, ocasionada pela produção anormal de espécies reativas de oxigênio (EROs), as principais injúrias. Desta maneira, para se obter uma melhor qualidade seminal após a descongelação, é necessário adicionar aos diluentes seminais elementos que desempenhem função antioxidante, visando conter o aumento dos níveis dos agentes oxidantes. Coenzima Q10 (CoQ10) é um agente lipossolúvel promotor de energia, tendo como principal função transportar prótons e elétrons no processo de síntese de ATP na membrana mitocondrial interna, através da cadeia de transporte de elétrons. Ainda, a CoQ10 atua como um potente antioxidante em diversos sistemas biológicos, tais como, lipoproteínas e membranas, protegendo-os contra a oxidação, inibindo a formação de hidroperóxidos e, consequentemente, prevenindo a peroxidação lipídica. Desta forma, o objetivo deste estudo foi avaliar a ação da coenzima Q10 (CoQ10) no espermatozoide de garanhões resistentes (RC) e sensíveis (SC) a congelação. Cada ejaculado (n=24) foi dividido em nove tratamentos e submetido à congelação,... (Resumo completo, clicar acesso eletrônico abaixo)
Doutor
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Silva, Fabiana Barreiro de Freitas [UNESP]. "Efeito protetor da coenzima Q10 sobre os danos oxidativos da L-Tiroxina no músculo sóleo de ratos: Fabiana Barreiro de Freitas Silva. -". Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/124446.
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000836295.pdf: 546084 bytes, checksum: 707b6f452fbf564a1f958ea9e2517ddd (MD5)Os músculos esqueléticossão tecidos dinâmicos que podem alterar suas características fenotípicas proporcionando melhor adaptação funcional com estímulos variados. A habilidade de adaptação do tecido muscular durante o crescimento e exercício é dependente de mudanças qualitativas e quantitativas na expressão induzida pelos diversos estímulos. A L-tiroxina é um hormônio produzido pela glândula tireoide e tem sido utilizada como modelo experimental para estimulação de estresse oxidativo no músculo esquelético. A Coenzima Q10 (CoQ10) é uma provitamina lipossolúvel sintetizada endogenamente e naturalmente encontrada em alimentos como a carne vermelha, peixes, cereais, brócolis e espinafre. Apresenta propriedade antioxidante e potencial no tratamento de doenças degenerativas e neuromusculares. No presente trabalho foi avaliado o efeito protetor da CoQ10 no músculo sóleo frente aos danos provocados pela L- tiroxina. Os ratos foram distribuídos em quatro Grupos de seis animais cada: Grupo 1 (G1, controle); Grupo 2 (G2, coenzima Q10); Grupo 3 (G3, L-tiroxina) e Grupo 4 (G4, coenzima Q10 e L-tiroxina). Após a eutanásia, o sangue dos animais foi colhido e foi analisada a atividade sérica das enzimas creatina quinase (CK) e aspartato aminotransferase (AST). No homogenato do músculo sóleo foram avaliados fatores relacionados ao estresse oxidativo. A CoQ10 protegeu o músculo sóleo e favoreceu a manutenção da atividade das enzimas antioxidantes glutationa redutase e glutationa peroxidase, da concentração de glutationa reduzida e oxidada, além de evitar a lipoperoxidação. Os resultados indicam que a CoQ10 protege o músculo sóleo de ratos dos danos oxidativos provocados pela L-tiroxina.
Skeletal muscles are dynamic tissues that can alter their phenotypic characteristics providing better functional adaptation to different stimulus.The hability to adapt the muscle tissue during growth and exercise is dependent on qualitative and quantitative changes in expression induced by various stimuli. L-thyroxine is a hormone produced by the thyroid gland and has been used as an experimental model for stimulation of oxidative stress in skeletal muscle.CoQ10 is a fat-soluble provitamin endogenously synthesized and naturally found in foods like red meat, fish, grains, broccoli and spinach.Features antioxidant properties and potential in the treatment of degenerative diseases and neuromuscular diseases.The present study evaluated the protective effect of CoQ10 in the soleus muscle against damage caused by L-thyroxine .The rats were divided in to four groups of six animals each: Group 1(G1, Control); Group 2(G2, coenzyme Q10); Group 3 (G3, L-thyroxine) and Group 4 (G4, coenzyme Q10 and L -thyroxine) .After euthanasia, blood was collected and serum was analyzed activity of the enzymes creatine kinase (CK) and aspartate aminotransferase (AST).In the soleus muscle homogenate factors related to oxidative stress were evaluated. CoQ10 protected the soleus muscle and favored the maintenance of the antioxidant enzymes glutathione reductase and glutathione peroxidase, the concentration of reduced and oxidized glutathione, and prevent lipid peroxidation. The results indicate that CoQ10 protects rat soleus muscle from oxidative damage caused by L- thyroxine
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Silva, Fabiana Barreiro de Freitas. "Efeito protetor da coenzima Q10 sobre os danos oxidativos da L-Tiroxina no músculo sóleo de ratos / Fabiana Barreiro de Freitas Silva. -". Araçatuba, 2014. http://hdl.handle.net/11449/124446.
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Orientador: Fábio Ermínio MingattoBanca:Elisa Maria de Sousa Russo
Banca: Luzia Helena Queiroz
Resumo: Os músculos esqueléticossão tecidos dinâmicos que podem alterar suas características fenotípicas proporcionando melhor adaptação funcional com estímulos variados. A habilidade de adaptação do tecido muscular durante o crescimento e exercício é dependente de mudanças qualitativas e quantitativas na expressão induzida pelos diversos estímulos. A L-tiroxina é um hormônio produzido pela glândula tireoide e tem sido utilizada como modelo experimental para estimulação de estresse oxidativo no músculo esquelético. A Coenzima Q10 (CoQ10) é uma provitamina lipossolúvel sintetizada endogenamente e naturalmente encontrada em alimentos como a carne vermelha, peixes, cereais, brócolis e espinafre. Apresenta propriedade antioxidante e potencial no tratamento de doenças degenerativas e neuromusculares. No presente trabalho foi avaliado o efeito protetor da CoQ10 no músculo sóleo frente aos danos provocados pela L- tiroxina. Os ratos foram distribuídos em quatro Grupos de seis animais cada: Grupo 1 (G1, controle); Grupo 2 (G2, coenzima Q10); Grupo 3 (G3, L-tiroxina) e Grupo 4 (G4, coenzima Q10 e L-tiroxina). Após a eutanásia, o sangue dos animais foi colhido e foi analisada a atividade sérica das enzimas creatina quinase (CK) e aspartato aminotransferase (AST). No homogenato do músculo sóleo foram avaliados fatores relacionados ao estresse oxidativo. A CoQ10 protegeu o músculo sóleo e favoreceu a manutenção da atividade das enzimas antioxidantes glutationa redutase e glutationa peroxidase, da concentração de glutationa reduzida e oxidada, além de evitar a lipoperoxidação. Os resultados indicam que a CoQ10 protege o músculo sóleo de ratos dos danos oxidativos provocados pela L-tiroxina.
Abstract: Skeletal muscles are dynamic tissues that can alter their phenotypic characteristics providing better functional adaptation to different stimulus.The hability to adapt the muscle tissue during growth and exercise is dependent on qualitative and quantitative changes in expression induced by various stimuli. L-thyroxine is a hormone produced by the thyroid gland and has been used as an experimental model for stimulation of oxidative stress in skeletal muscle.CoQ10 is a fat-soluble provitamin endogenously synthesized and naturally found in foods like red meat, fish, grains, broccoli and spinach.Features antioxidant properties and potential in the treatment of degenerative diseases and neuromuscular diseases.The present study evaluated the protective effect of CoQ10 in the soleus muscle against damage caused by L-thyroxine .The rats were divided in to four groups of six animals each: Group 1(G1, Control); Group 2(G2, coenzyme Q10); Group 3 (G3, L-thyroxine) and Group 4 (G4, coenzyme Q10 and L -thyroxine) .After euthanasia, blood was collected and serum was analyzed activity of the enzymes creatine kinase (CK) and aspartate aminotransferase (AST).In the soleus muscle homogenate factors related to oxidative stress were evaluated. CoQ10 protected the soleus muscle and favored the maintenance of the antioxidant enzymes glutathione reductase and glutathione peroxidase, the concentration of reduced and oxidized glutathione, and prevent lipid peroxidation. The results indicate that CoQ10 protects rat soleus muscle from oxidative damage caused by L- thyroxine
Mestre
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Burgos, Rafael Ramos de 1981. "Influência da nifedipina e da coenzima Q10 no processo de degeneração/regeneração muscular em camundongos mdx". [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317504.
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Orientador: Elaine MinatelDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Tratamentos com antioxidantes e bloqueadores de canais de cálcio têm apresentado resultados positivos na diminuição da mionecrose nas fibras musculares distróficas. O objetivo do presente projeto foi verificar se o tratamento com o bloqueador de cálcio Nifedipina (Ni) e o antioxidante Coenzima Q10 (CoQ10), administrados isoladamente ou em associação antes que se iniciem os ciclos de degeneração/regeneração muscular, pode apresentar efeito benéfico sobre as fibras musculares distróficas de camundongos mdx, modelo experimental da distrofia muscular de Duchenne. Camundongos mdx com 14 dias de vida pós-natal foram divididos em 4 grupos experimentais: (1) tratados com álcool 20% e solução aquosa 1% de Tween 80; (2) tratados com a associação de Ni e CoQ10; (3) tratados com Ni isoladamente; (4) e tratados com somente CoQ10. Camundongos da linhagem C57BL/10 foram usados como controle. Os músculos tibial anterior (TA), diafragma (DIA) e esternomastóideo (STN) foram retirados e utilizados para quantificar: (1) o número de fibras em degeneração, regeneradas e normais; (2) o nível de TNF-?, NF-?B e 4-HNE; (3) o conteúdo de cálcio total; e (4) a área de inflamação muscular. Amostras de sangue foram utilizadas para determinação dos níveis creatina quinase (CK). Os animais tratados com Ni apresentaram: redução significativa de fibras em degeneração no músculo TA, redução nos níveis de TNF-? em todos os músculos analisados e no conteúdo de NF-?B e cálcio no músculo DIA. Animais mdx tratados com Coenzima Q10 mostrou redução: CK, TNF-? no músculo TA, no conteúdo de NF-?B nos músculos DIA e STN, na área de inflamação no músculo DIA e determinação do cálcio nos músculos DIA e STN. A associação dos tratamentos demonstrou redução significativa na análise de CK, no TNF-? do músculo TA, na área de inflamação, conteúdo do NF-?B e cálcio no músculo DIA. O conjunto dos resultados sugere que a Ni e a CoQ10 possam ser potencialmente úteis para o tratamento farmacológico da distrofinopatias. Entretanto, estudos futuros da dosagem e do tempo de tratamento serão necessários para obtenção de efeitos benéficos mais significativos sobre os músculos distróficos
Abstract: Treatment using antioxidant and calcium channel blockers have shown positive results for myonecrosis decrease in dystrophic muscle fibers. The aim of this study is to verify if treatment with Nifedipine (Ni) calcium channel blocker and Coenzyme Q10 (CoQ10) antioxidant, administered alone or in association before degeneration/regeneration cycles take place, may have a beneficial effect on dystrophic muscle fibers in mdx mice, which are the experimental model for Duchenne's dystrophy. Mdx mice at 14 days old were divided into 4 experimental groups: (1) treated with 20% alcohol and 1% Tween 80 water solution; (2) treated with an association of Ni and CoQ10; (3) treated with Ni alone; and (4) treated with CoQ10 alone. C57BL/10 mice were used as a control. The tibialis anterior (TA), diaphragm (DIA) and sternomastoid (STN) muscles were removed and used for quantification of: (1) number of degenerated, regenerated and wild-type fibers; (2) TNF-?, NF-?B and 4-HNE levels; (3) total amount of calcium; and (4) muscle inflammation area. Creatine kinase (CK) was analyzed from a blood sample. The animals treated with Ni showed: a significant decrease of degenerated muscle fibers in the TA muscle, a reduced TNF-? level in all muscles analyzed and lower levels of NF-?B and calcium in the DIA muscle. Mdx mice treated with Coenzyme Q10 presented a decrease of the following: CK expression, TNF-? level in the TA muscle, NF-?B level in the DIA and STN muscles, inflammation area in the DIA muscle and calcium content in the DIA and STN muscles. The association of both drugs showed a significant reduction of CK in the blood, TNF-? in the TA muscle, and also a reduction of the inflammation area, the NF-?B expression and the calcium content of the DIA muscle. Overall results suggest that Ni and CoQ10 may play a potential role as a pharmacological treatment for dystrophynopathies. However, further studies must be carried out for both dosage and treatment period to obtain more significant beneficial effects on dystrophic muscles
Mestrado
Anatomia
Mestre em Biologia Celular e Estrutural
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Buján, Murlà Núria. "Estudis bioquímics i moleculars en pacients amb deficiències mitocondrials i de coenzim Q10". Doctoral thesis, Universitat de Girona, 2016. http://hdl.handle.net/10803/398580.
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The diagnose of a mitochondrial disease implies biochemical studies such as the enzymatic activities of the mitochondrial respiratory chain (MRC) and the quantification of the amount of CoQ10 in energetic tissues. Throughout this thesis we have worked on the development of methods to improve these studies in order to get a better diagnostic efficiency in these patients. Blue Native electrophoresis gel allows the study of complex V ATPasa activity and complex I enzymatic activity in cultured fibroblasts, which are not possbile to be studied using standard spectrophotometric methods, becoming good complementary assays. Patients with primary CoQ10 deficiencies improve with CoQ10 treatment. We have developed a technique for the study of the endogenous CoQ10 biosynthesis in cells using non-radioactive isotops that discriminates primary from secondary CoQ10 deficiencies.The implemented methodologies have improved the quality of the analysis test and the diagnose in patiens with a supect of mitochondrial disease or CoQ10 deficiecyEl diagnòstic de les malalties mitocondrials inclou estudis bioquímics com ara les activitats enzimàtiques dels complexes de la cadena respiratòria mitocondrial (CRM) i la quantificació del CoQ10 en teixits energètics. En aquesta tesi s’ha treballat en el desenvolupament de mètodes d’estudi per millorar el rendiment diagnòstic dels pacients. La electroforesis en Blue Native-gel permet l’estudi de l’activitat ATPasa del complex V i l’activitat del complex I en fibroblasts, activitats que no es poden determinar mitjançant les tècniques espectrofotomètriques habituals, esdevenint una bona tècnica complementària als estudis espectrofotomètrics. Els pacients amb deficiències primàries de CoQ10 milloren amb tractament amb CoQ10. Hem desenvolupat una tècnica d’estudi de la via de biosíntesi endògena de CoQ10 en cèl•lules mitjançant isòtops no-radioactius que permet discriminar entre deficiències primàries i secundàries de CoQ10. Les metodologies implementades han millorat la qualitat analítica i el diagnòstic en pacients amb sospita de malaltia mitocondrial i/o deficiència de CoQ10
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SABBATINELLI, JACOPO. "Impatto della supplementazione con Ubiquinolo sulla funzione endoteliale in soggetti a rischio di sviluppare patologie cardiovascolari: studio clinico spontaneo, in doppio cieco, randomizzato, controllato con placebo, a gruppi paralleli". Doctoral thesis, Università Politecnica delle Marche, 2018. http://hdl.handle.net/11566/252542.
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La maggior parte dei fattori di rischio cardiovascolari si traduce in un'aumentata produzione di specie reattive dell'ossigeno (ROS), che a loro volta causano disfunzione endoteliale riducendo la biodisponibilità del mediatore vasodilatante ossido nitrico (NO). È noto che la supplementazione con Coenzima Q10 (CoQ10) migliora la performance cardiaca nello scompenso congestizio e nella cardiopatia ischemica, ed inoltre diminuisce significativamente la pressione arteriosa.
Un trial clinico in doppio-cieco, randomizzato, a gruppi paralleli, è stato condotto su 51 soggetti con rischio cardiovascolare moderato e disfunzione endoteliale per comprendere gli effetti della supplementazione con ubichinolo sulla funzione endoteliale, misurata attraverso la determinazione ecografica non invasiva della flow-mediated dilation (FMD). I soggetti sono stati randomizzati in due gruppi di trattamento (ubichinolo, 100 mg o 200 mg/die) e un gruppo placebo. Durante ciascuna visita (T0, 4 e 8 settimane), sono stati misurati pressione arteriosa e FMD, parametri sieroematici (compreso il profilo lipidico), livelli plasmatici di CoQ10 ossidato/ridotto, NO e perossinitrito.
La somministrazione di ubichinolo ha aumentato fortemente i livelli plasmatici di CoQ10 totale e ridotto. I soggetti assegnati ad entrambi i gruppi di trattamento hanno mostrato un incremento nella FMD, senza differenze significative tra i due dosaggi. Tuttavia, in seguito all'analisi di biodisponibilità plasmatica di CoQ10, è stata dimostrata una relazione positiva tra l'incremento di FMD e il miglioramento dello stato ossidativo del CoQ10. Nessuna variazione significativa del profilo lipidico è stata riscontrata nei soggetti trattati. Un aumento dose-dipendente dei livelli plasmatici di NO è stato osservato nei soggetti trattati dopo 8 settimane. Esiste una correlazione positiva tra FMD e livelli di NO e, dunque, tra questi ultimi e la funzione endoteliale.
La FMD e lo stato ossidativo plasmatico migliorano significativamente dopo somministrazione di ubichinolo. La biodisponibilità dell'ubichinolo si correla positivamente ai miglioramenti della FMD. Inoltre, l'influenza positiva della supplementazione con CoQ10 è indipendente dal profilo lipidico plasmatico, suggerendo un possibile effetto diretto dell'ubichinolo sulle cellule endoteliali.Most of the major cardiovascular risk factors are characterized by an increased production of reactive oxygen species (ROS), leading to endothelial dysfunction through breakdown of the vasodilating compound nitric oxide (NO). Supplementation with Coenzyme Q10 (CoQ10) positively affects heart performance in congestive heart failure and ischemic heart disease, along with a significant blood pressure lowering effect. To understand the effects of ubiquinol supplementation on endothelial function, measured through non-invasive ultrasonographic assessment of flow-mediated dilation (FMD), a double-blind, randomized, parallel-groups clinical trial was carried out on 51 subjects with moderate cardiovascular risk and endothelial dysfunction. Subjects were randomized to receive ubiquinol, 100 or 200 mg daily, or placebo. During each visit (T0, 4-weeks, 8-weeks) blood pressure, FMD, hematologic parameters (including lipid profile), reduced/oxidized CoQ10 levels, NO and peroxynitrite plasma levels were evaluated. Ubiquinol administration strongly improved total and reduced CoQ10 plasma levels. Subjects assigned to both treatment groups showed an increased FMD compared with subjects in placebo group, with no significant difference between the two dosages. However, after CoQ10 plasma bioavailability analysis, a positive relationship between FMD increases and CoQ10 oxidative status improvements was demonstrated. No significant change in lipid profile was observed in treated subjects. A significant dose-dependent increase in NO plasma levels was observed in treated subjects after T2. NO plasma levels are positively related to FMD and, thus, to endothelial function. FMD and plasma oxidative status are significantly improved following administration of ubiquinol. Bioavailability of ubiquinol is positively correlated with FMD improvements. Positive influence of CoQ10 supplementation is independent from plasma lipid profile, suggesting a direct effect of ubiquinol on endothelial cells.
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Bandeira, Rafael dos Santos. "Adição de piruvato e coenzima Q10 ao diluente à base de leite desnatado para refrigeração do sêmen equino". Botucatu, 2019. http://hdl.handle.net/11449/182407.
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Orientador: José Antônio Dell'Aqua JúniorResumo: O espermatozoide exige um fornecimento constante de energia para a manutenção de suas funções celulares e quando desafiado por processos de criopreservação do sêmen, sofrem danos irreversíveis. Para o desenvolvimento de técnicas que visam o aumento da longevidade espermática, é necessário considerar que mesmo em metabolismo basal, o espermatozoide necessita de substratos para garantir sua motilidade e poder fecundante após a ejaculação. Para atender suas demandas energéticas, estudos recomendam o uso de nutrientes exógenos, como o piruvato de sódio e a coenzima Q10 (CoQ10), substratos fundamentais na bioenergética celular. Visto a importância da refrigeração de sêmen em garanhões e o potencial destas substâncias em melhorar os parâmetros seminais atuando como substrato energético e antioxidante, respectivamente, o presente trabalho tem por objetivo abordar aspectos relacionados ao metabolismo espermático, bem como o papel do piruvato e CoQ10 visando minimizar os efeitos deletérios da refrigeração sobre a qualidade do sêmen equino. Foram adicionadas diferentes concentrações de piruvato de sódio e da CoQ10 ao sêmen de garanhões considerados “good coolers” (GC) e “bad coolers” (BC). Primeiramente, foram estabelecidas as concentrações mais eficazes de piruvato e CoQ10 no diluente de refrigeração BotuSêmen® (Botupharma Botucatu/SP Brasil) para preservar os parâmetros espermáticos na refrigeração a 5° C por até 48 horas. Foi utilizado 1 ejaculado de 25 garanhões das raças Quarto de... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The spermatozoa require a constant supply of energy for the maintenance of their cellular functions and when challenged by processes of cryopreservation of the semen, they suffer irreversible damages. For the development of techniques that aim to increase sperm longevity, it is necessary to consider that even in basal metabolism, the spermatozoa require substrate to ensure their motility and fertilizing power after ejaculation. To attend their energy demands, studies recommend the use of exogenous nutrients, such as sodium pyruvate and coenzyme Q10 (CoQ10), key substrates in cellular bioenergetics. Considering the importance of semen cooling in stallions and the potential of these substances to improve seminal parameters acting as an energetic and antioxidant substrate, this review aims to address aspects related to cooling, as well as the role of sodium pyruvate and CoQ10 in minimizing the effects of cooling on the quality of equine semen. Different concentrations of sodium pyruvate and CoQ10 have been added to semen from good coolers (GC) and bad coolers (BC). First, the most effective concentrations of sodium pyruvate and CoQ10 in the BotuSêmen® extender (Botupharma Botucatu / SP Brazil) were established to preserve the sperm parameters at 5°C for up to 48 hours. Each ejaculate was split into 7 treatments, with sodium pyruvate and CoQ10 being added at concentrations of 1 mmol/l (P1), 2 mmol/l (P2), 3 mmol/l sodium pyruvate (P3), 25 µmol/l (Q25), 50 µmol/l (Q50) and 75 µmol... (Complete abstract click electronic access below)
Mestre
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LIMA, Roberto Albuquerque. "Produção de Biossurfactante, Coenzima Q10 e lipídeos poliinsaturados (ω3 e ω6) por amostras de Candida glabrata (UCP 1002 e 1556) utilizando resíduos agroindustriais". Universidade Federal de Pernambuco, 2014. https://repositorio.ufpe.br/handle/123456789/19684.
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Capes
Avanços tecnológicos buscam recursos naturais adequados e disponíveis para obtenção de produtos sustentáveis e economicamente viáveis. Neste trabalho foi estudada a produção de metabólitos como os biossurfactante, lipídeos e Coenzima Q10 por Candida glabrata (UCP 1002 e 1556), por processo biotecnológico. O cultivo foi realizado em meio de baixo custo a base de resíduos agroindustriais (milhocina e soro de leite). Inicialmente neste estudo foi realizado um processo de produção de biossurfactante por C. glabrata (UCP 1002 e 1556), utilizando resíduos agroindustriais como fonte de carbono e nitrogêncio em substituição ao meio sintético, sendo observado que as duas linhagens produziram similares quantidades de biossurfactante. Foi realizado um processo de otimização do meio a base de resíduos agroindustriais por Delineamento Composto Central (DCC) 22. Os resultados obtidos evidenciaram que no segundo planejamento com 40% de soro de leite e 20% de milhocina foi mais eficiente na produção de biossurfactante utilizando a C. glabrata 1556, com uma redução da tensão superficial de 72 para 28,8mN/m. O biossurfactante foi caracterizado e classificado como lipoproteína e além disso demonstrou se seu caráter aniônico. O meio otimizado empregou se na produção e caracterização da CoQ10 por C. glabrata (UCP 1556), ficando evidenciado a presença significativa do composto e sua ação antioxidante. Neste meio foi testado o potencial das duas linhagens de C. glabrata (UCP 1002 e 1556) na produção de lipídeos e ácidos graxos poliinsaturados (PUFAs) e uma quantidade elevada de ácido γ-ácido linolênico (ω6) e α-ácido linolênico (ω3) foi detectada. Os resíduos agroindustriais são substratos nutritivos que representam uma redução econômica para a produção compostos limpos que podem ser aplicados na indústria de cosmética e farmacêutica.
Technological advances seek appropriate natural resources and available for achieving of sustainable products and viable economically. In this work was studied the production of metabolites as biosurfactant, Coenzyme Q10 and lipids by Candida glabrata (UCP 1002 and 1556) for biotechnological process. The cultivation was carried in medium of low cost the base of agroindustrial waste (whey and corn steep liquor). Initially this study was performed a process of biosurfactant production by C. glabrata (UCP 1002 and 1556), using agroindustrial residues as a carbon source and nitrogen replacing the synthetic medium, it was observed that both strains produced similar amounts of biosurfactant. It was performed a optimization process of the medium the base of agroindustrial waste by Central Composite Design (CCD) 22. The results showed that the second planning with 40% of whey and 20% of corn steep liquor it was more efficient in the biosurfactant production using C. glabrata (UCP 1556), with a reduction in surface tension from 72 to 28,8mN/m. The biosurfactant was characterized and classified as lipoprotein and furthermore it was demonstrated its anionic character. The optimized medium was performed in the production and characterization of CoQ10 by C. glabrata (UCP 1556), getting evidenced the significant presence of the compound and its antioxidant action. In this medium was tested the potential of two strains of C. glabrata (UCP 1002 e 1556) in the production of lipids and polyunsaturated fatty acids (PUFAs) and a high quantity of γ-linoleic acid (ω6) and e α- linoleic acid (ω3) was detected. The agroindustrial wastes are nutritious substrates which represent an economic cost reduction in the production of clean compounds that it can be applied in cosmetic and pharmaceutical industry.
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CALDERAN, CRISTINA. "SVILUPPO DI MODELLI DI LIEVITO PER LA VALIDAZIONE DI NUOVE MUTAZIONI PATOGENICHE ASSOCIATE AD ANEURISMA DELL'AORTA TORACICA E DEFICIT PRIMARIO DI COENZIMA Q10". Doctoral thesis, Università degli studi di Padova, 2023. https://hdl.handle.net/11577/3469813.
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The yeast Saccharomyces cerevisiae is a cheap, time-saving and versatile tool to study human genetic diseases, since a great number of genes and biological processes are evolutionarily conserved. Moreover, residues at which mutations occur in human are often conserved in yeast. Not least, yeast can grow either by mitochondrial-dependent respiration or by ethanol fermentation, thus permitting to study mitochondrial diseases. We employed this model organism to test the functional effect of novel α-smooth muscle actin (ACTA2) heterozygous mutations, found in patients with familial thoracic aortic aneurysm and/or dissection (TAAD) and novel COQ4 autosomal recessive mutations associated with primary CoQ10 deficiency.
ACTA2 is a major component of thin filaments of the contraction units of smooth muscle cells (SMCs). Polymerized fibers of ACTA2 filaments interact with myosin, regulating blood pressure and flow, and maintaining the structural integrity of blood vessels. Autosomal dominant missense mutations in the ACTA2 gene are the most common cause of familial non-syndromic TAAD, responsible for 14% of the cases. However, ACTA2 mutations are inherited with reduced penetrance (about 0,5) and variable expressivity with respect to the age of onset and the degree of aortic dilation. In addition, TAAD-associated ACTA2 genetic defects are thought to act by a dominant-negative mechanism and not through haploinsufficiency. Hence the importance of developing a system to functionally validate variants identified during patients screening. Here we report the development of a yeast model that allowed us to validate the pathogenicity of five novel human ACTA2 missense variants, found in TAAD patients. Furthermore, our data proved in vivo that TAAD-associated mutant actin isoforms exert a dominant negative effect on wild type actin, impairing its functionality.
Next, we analysed COQ4 mutations found in patients suffering from primary CoQ10 deficiency, a rare mitochondrial disease caused by mutations in COQ genes, involved in Coenzyme Q biosynthesis. Clinical phenotypes of patients range from a fatal multisystem disease to isolated steroid resistant nephrotic syndrome or isolated central nervous system disease. In yeast and in mammalian cells, COQ proteins have been well characterized, but the role of some of them is not completely clear yet. For example, the precise function of COQ4 is unknown, even if it seems to have a key structural role for the formation and stability of the Coq polypeptide complex assembly, necessary for CoQ biosynthesis. Mutations in the COQ4 gene in most cases cause a lethal neonatal mitochondrial encephalomyopathy, but the clinical phenotype of patients and the age of onset vary widely, making diagnosis more difficult. By means of a recombinant yeast model we validated the pathogenicity of all tested COQ4 mutations; moreover, our findings support the putative central role of the COQ4 polypeptide in CoQ10 production.
Yeast based assays described here provide a simple tool for validating new putative pathogenic ACTA2 or COQ4 variants, in order to perform a prompt diagnosis and institute a treatment as early as possible.The yeast Saccharomyces cerevisiae is a cheap, time-saving and versatile tool to study human genetic diseases, since a great number of genes and biological processes are evolutionarily conserved. Moreover, residues at which mutations occur in human are often conserved in yeast. Not least, yeast can grow either by mitochondrial-dependent respiration or by ethanol fermentation, thus permitting to study mitochondrial diseases. We employed this model organism to test the functional effect of novel α-smooth muscle actin (ACTA2) heterozygous mutations, found in patients with familial thoracic aortic aneurysm and/or dissection (TAAD) and novel COQ4 autosomal recessive mutations associated with primary CoQ10 deficiency. ACTA2 is a major component of thin filaments of the contraction units of smooth muscle cells (SMCs). Polymerized fibers of ACTA2 filaments interact with myosin, regulating blood pressure and flow, and maintaining the structural integrity of blood vessels. Autosomal dominant missense mutations in the ACTA2 gene are the most common cause of familial non-syndromic TAAD, responsible for 14% of the cases. However, ACTA2 mutations are inherited with reduced penetrance (about 0,5) and variable expressivity with respect to the age of onset and the degree of aortic dilation. In addition, TAAD-associated ACTA2 genetic defects are thought to act by a dominant-negative mechanism and not through haploinsufficiency. Hence the importance of developing a system to functionally validate variants identified during patients screening. Here we report the development of a yeast model that allowed us to validate the pathogenicity of five novel human ACTA2 missense variants, found in TAAD patients. Furthermore, our data proved in vivo that TAAD-associated mutant actin isoforms exert a dominant negative effect on wild type actin, impairing its functionality. Next, we analysed COQ4 mutations found in patients suffering from primary CoQ10 deficiency, a rare mitochondrial disease caused by mutations in COQ genes, involved in Coenzyme Q biosynthesis. Clinical phenotypes of patients range from a fatal multisystem disease to isolated steroid resistant nephrotic syndrome or isolated central nervous system disease. In yeast and in mammalian cells, COQ proteins have been well characterized, but the role of some of them is not completely clear yet. For example, the precise function of COQ4 is unknown, even if it seems to have a key structural role for the formation and stability of the Coq polypeptide complex assembly, necessary for CoQ biosynthesis. Mutations in the COQ4 gene in most cases cause a lethal neonatal mitochondrial encephalomyopathy, but the clinical phenotype of patients and the age of onset vary widely, making diagnosis more difficult. By means of a recombinant yeast model we validated the pathogenicity of all tested COQ4 mutations; moreover, our findings support the putative central role of the COQ4 polypeptide in CoQ10 production. Yeast based assays described here provide a simple tool for validating new putative pathogenic ACTA2 or COQ4 variants, in order to perform a prompt diagnosis and institute a treatment as early as possible.
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Wainwright, Luke. "Mechanisms of coenzyme Q10 blood-brain barrier transport". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10060760/.
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Coenzyme Q10 (CoQ10) deficiencies are unique among mitochondrial respiratory chain (MRC) disorders in that they are potentially treatable. While there is clear evidence, both clinically and biochemically, for the improvement of peripheral abnormalities associated with CoQ10 deficiency following CoQ10 supplementation, neurological symptoms are only partially ameliorated. The reasons for the refractory nature of the neurological sequelae associated with a CoQ10 deficiency are as yet unknown and may be a consequence of irreversible damage prior to CoQ10 supplementation, the retention of CoQ10 in the blood-brain barrier (BBB) itself, or simply reflect poor transport of CoQ10 across the BBB. This thesis presents the first isolated investigations into the mechanisms that govern bi-directional BBB transport of CoQ10 and its synthetic analogue, idebenone, using normal and pathophysiological cell models relevant to disorders of CoQ10 biosynthesis. The mouse BBB endothelial cell line bEnd.3 and porcine primary brain endothelial cells (PBECs) co-cultured with primary astrocytes were used to assess transcytosis from 'blood-to-brain' or 'brain-to-blood', revealing that although CoQ10 can traverse the BBB, CoQ10 is being effluxed back to the blood, which could explain the refractory nature of CoQ10 therapy, whereas, idebenone appeared to cross the BBB passively. Using inhibitors of known transport systems for lipoproteins, the circulatory bio-carriers of CoQ10 in vivo, three systems mediating the BBB transport of lipoprotein-bound CoQ10 were identified. Inhibitors of the scavenger receptor class B type 1 (SR-B1), BLT-1, and the receptor for advanced glycation end products (RAGE), FPS-ZM1, reduced uptake of lipoprotein-bound CoQ10 towards the brain, implicating RAGE and SR-B1 as modes for CoQ10 brain uptake. In the reverse direction, the low-density lipoprotein receptor-related protein-1 (LRP-1) inhibitor, RAP, reduced efflux of lipoprotein-bound CoQ10 towards the blood, implicating LRP-1 as a major impediment to brain entry of CoQ10. This study is the first to generate a BBB endothelial cell model of CoQ10 deficiency, using para-aminobenzoic acid (pABA) to pharmacologically induce a depletion of cellular CoQ10 status, resulting in a global reduction of MRC enzyme activities. The CoQ10 deficient BBB models were leakier to large permeability markers, with poor BBB tight-junction formation, and altered CoQ10 transport dynamics in favour of an increased net efflux towards the blood, suggesting BBB pathophysiology is key to the neurological presentation and refractory nature of CoQ10 supplementation in symptomatic patients. In addition, the effects of vitamin E, a common clinical co-therapy in the 'mito-cocktail', and simvastatin were assessed. Interestingly, vitamin E co-administration reduced net efflux of CoQ10 from the brain. It is unknown why this occurs, but oxidative effects on the BBB transporters and/or carrier-lipoproteins may be factors to consider. In-line with its deleterious effect on CoQ10 biosynthesis, simvastatin therapy appeared to disrupt BBB integrity, increasing the paracellular leak of the BBB. This would be detrimental to normal brain homeostasis, particularly given the BBBs major role in limiting brain entry of the small molecule plasma excitotoxins, calcium, and glutamate. Throughout this study CoQ10 was quantified using a novel and rapid mass spectrometric method (ESI+ LC-MS/MS), which could potentially enable detection of CoQ10 in the CSF of patients presenting with neurological symptoms, perhaps providing a new analytical tool for the diagnosis of CoQ10 deficiencies in clinical laboratories. In conclusion, this thesis has demonstrated for the first time the pathophysiological consequences of a CoQ10 deficiency on the BBB. It has highlighted the impact of a deficit in CoQ10 status on CoQ10 delivery to the brain parenchyma and has elucidated some of the mechanisms by which CoQ10 is transported across the BBB, which are ultimately dictated by lipoprotein interactions. Additionally, this thesis outlines the potential dangers of statin therapy in patients with an underlying or established MRC dysfunction. Overall, this thesis provides insights into the limitations of CoQ10 supplementation as a therapy for neurological disorders associated with MRC dysfunction and indicates that further work will be required to improve the delivery of exogenous CoQ10 across the BBB, alongside a need for further investigations into the composition of the widely administered 'mito-cocktail'.
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Yoo, Harrison, Amanda Teague e Charles C. Collins. "DISSOLUTION ANALYSIS OF OTC COENZYME Q10 DIETARY SUPPLEMENTS". Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/28.
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Introduction: Coenzyme Q10 (CoQ10) is a fat-soluble substance (ubiquinone) which has a bright orange color in appearance and is widely distributed (ubiquitous) in animals and many bacteria. CoQ10’s presence is most prevalent in mitochondria and it is involved in aerobic cellular respiration and aides in converting ingested nutrients into a readily accessible form of energy, specifically ATP (adenosine triphosphate). CoQ10 is supplied through our diets and can be found more in dark leafy green vegetables, fish and organ meats. CoQ10 supplementation should be beneficial due to its characteristic antioxidant scavenging of free radicals that our body produces while in the cellular respiration process for generating energy from nutrients. Although CoQ10 has great antioxidant benefit, a challenge remains for supplement manufacturers to deliver a sufficient does of this sparingly soluble molecule. Dietary supplements do not have the significant FDA oversight that exists for legend drugs, resulting in significant variability within and between brands. The main hypothesis of this project is that commercially available CoQ10 supplements don’t deliver a sufficient mass of CoQ10 when compared to the labelled quantity. Methods: To test this hypothesis, the group purchased and tested 14 commercially available CoQ10 supplements with each serving containing 100 mg of active, choosing a variety of drug delivery systems (DDS) and also included one in-house product, which contained 70 mg of active. The DDSs examined consisted of 7 soft shell gelatin (SSG) capsules (the most common type available), 3 hard shell gelatin (HSG) capsules, 3 tablets (tab), 1 powder, and 1 suspension. Each DDS was placed into a 500 mL volumetric flask (VF) into an aqueous of 0.1 N HCl acid and 0.1% Tween 80, using a standard FDA dissolution method. To facilitate drug release, the contents were removed from the HSG capsules; the SSG capsules were perforated; and the tabs were broken/crushed. After this, a magnetic stir bar was placed into each flask and all DDS samples were vigorously stirred for 30-45 minutes, including being inverted every 10 minutes to further facilitate dissolution of CoQ10 from each DDS. Filtered samples were obtained and the samples were analyzed by a reverse-phase High Performance Liquid Chromatography that was previously developed by this research group. Results and Conclusions: Only two of the 15 products evaluated had significant availability (mean > 50%) of CoQ10; one soft gelatin capsule (Product A, dissolved a mean of 68.57%), and the suspension (Product K, dissolved a mean of 56.71%). All of the other products averaged less than 4% dissolution of the labelled amount (range of values 0.19% to 3.64%). The in-house formulated HSG capsule (Product Q) released a mean amount equal to 8.11% of label (more than twice the percentage of the poorly performing commercial products). The consistency of the products was also variable, with product A having a range of 1.7 to 192 mg of CoQ10 released; Product K had a range of 35.8 to 76.1 mg of drug released. The group concluded that there are acceptable products available, but that most have significant performance issues.
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Gholipour, Ali-Farshad. "Symptomatische Effekte von Coenzym Q10 bei Morbus Parkinson". [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975019422.
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Yubero, Siles Dèlia. "Estudi del coenzim Q10 en pacients neuropediàtrics: avenços diagnòstics i identificació de noves causes d'alteracions secundàries". Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/398132.
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L’àrea de treball de la present tesi doctoral se situa en el context de les malalties genètiques del metabolisme energètic mitocondrial. Són malalties rares i hereditàries que afecten al conjunt de sistemes que fa servir l’organisme per incorporar i transformar els substrats en energia utilitzable per al correcte funcionament cel·lular. El coenzim Q10 és un component lipídic de totes les membranes cel·lulars que realitza un paper essencial a la cadena respiratòria mitocondrial, però també participa en moltes altres funcions cel·lulars, tan dins dels mitocondris com fora. En l’àmbit pediàtric, la deficiència de coenzim Q10 s’associa a estats de malaltia amb expressions fenotípiques heterogènies, i les causes que la expliquen poden ser primàries o bé secundàries (és a dir, per alteració dels gens implicats en la via de síntesi d’aquesta molècula –deficiència primària–, o per alteració d’altres gens no directament relacionats en la via biosintètica del coenzim Q10 –deficiència secundària). Aquesta deficiència bioquímica implica una disfunció del sistema de la fosforilació oxidativa mitocondrial, i normalment es manifesta de forma multiorgànica, alterant en major o menor grau els diferents òrgans, segons els nivells energètics que requereixen els teixits i d’altres factors no massa coneguts. L’objectiu principal d’aquesta tesi ha estat la millora del diagnòstic de pacients amb deficiències de coenzim Q10, a través de l’estudi sistemàtic d’aquest en diverses espècimens biològics i en associació amb dades clíniques, bioquímiques, histoquímiques, enzimàtiques i moleculars. A través de l’estudi i valoració de grans grups de pacients, s’ha pogut intuir la dinàmica d’aquesta molècula en certs tipus de malalties. Hem pogut descriure tres malalties que s’associen a una deficiència de coenzim Q10 de forma secundària, permetent que pacients afectats puguin beneficiar-se de la suplementació oral amb coenzim Q10, la qual ha demostrat millores clíniques de l’estat de pacients afectats amb patologies mitocondrials. També, hem realitzat avenços metodològics i tècnics, a nivell bioquímic i d’anàlisi de dades, que permetran abordar les classificacions actuals dels pacients amb malalties mitocondrials, en les quals és complicat assolir un diagnòstic molecular definitiu degut a la seva immensa complexitat.Mitochondrial diseases are genetic rare diseases which affect the energetic cellular system to obtain the required energy for basic survival. Coenzyme Q10 is a lipidic antioxidant located in all eukaryotic cellular membranes that is essential for mitochondrial respiratory chain activity, amongst other important roles not strictly related to mitochondrial function. Coenzyme Q10 deficiency is a biochemical trait defined by low coenzyme Q10 levels in tissues, which can manifest in five main classical phenotypes (from isolated nephropathies to fatal infantile multisystemic disease). The ethiology can be primary (when the genetic defect is in a gene affecting the coenzyme Q10 biosynthetic pathway) or secondary (when the altered gene is not directly related to the coenzyme Q10 biosynthesis), and this partially explains the high heterogeneity observed in these patients. The patophysiology is explained because there is a mitochondrial respiratory chain malfunction that affects the oxidative phosphorylation system and unbalances the antioxidant protection, consequently changing normal cellular behaviour. The main objective of this work has been to improve the diagnosis of patients with coenzyme Q10 deficiency, through the systematic analysis of various biological samples in association with clinical, biochemical, histochemical, enzymatic and molecular data. Through the study and evaluation of big cohorts of patients, we could establish that secondary coenzyme Q10 deficiencies are commoner than primary. Furthermore, we have reported an association of three different diseases with secondary coenzyme Q10 deficient states (GLUT-1 deficiency syndrome, pyrivate dehydrogenase deficiency, mucopolysaccharidosis type III), diseases that could benefit from coenzyme Q10 supplementation, which has demonstrated to produce clinical amelioration in mitochondrial patients. Finally, methodological improvements for coenzyme Q10 deficiency diagnosis were done through two different approaches. One is the analysis of coenzyme Q10 in urinary sediment to assess coenzyme Q10 levels of renal system cells, and the other one is the development of a statistical algorithm which shows the potential of coenzyme Q10 as a mitochondrial activity biomarker.
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Pietersen, Lauren. "Coenzyme Q10 for statin-induced myopathy : a systematic review". Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/71937.
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Thesis (MNutrition (ITE))--Stellenbosch University, 2012.ENGLISH ABSTRACT: Background Statins are drugs of known efficacy in the treatment of hypercholesterolaemia. However, statin-induced myopathy, an adverse effect of statins in up to 15% of its users, has warranted a reduction in the prescription dose or discontinuation of the drug. The exact mechanism of statin-induced myopathy is unknown, but the potential of Coenzyme Q10 (CoQ10) as treatment has been recognized due to decreased human plasma CoQ10 levels found after statin use and the concomitant role of CoQ10 in muscle function. Objectives This systematic review assessed the effect of CoQ10 supplementation on: the severity of statin-induced myopathic symptoms, levels of plasma creatine kinase, intramuscular and plasma CoQ10, as well as whether any adverse effects of CoQ10 supplementation such as abdominal pain, nausea and vomiting or headaches were experienced. Search methods Two searches for studies were conducted in The Cochrane Central Register of Controlled Trials (inception to March 2011 and inception to November 2011), MEDLINE (inception to March 2011 and inception to November 2011), Web of Science (inception to March 2011 and inception to November 2011), Science Direct (inception to March 2011 and inception to February 2012), Wiley Online Library (inception to March 2011 and inception to February 2012), Springerlink (inception to April 2011 and inception to February 2012), EBSCOhost [Academic Search Premier and CAB abstracts (inception to March 2011 and inception to February 2012), CINAHL (inception to March 2011 and inception to November 2011)], Scopus (inception to March 2011 and inception to November 2011) and Google Scholar (inception to March 2011 and inception to February 2012). Reference lists of articles were hand searched for relevant clinical trials. Only trials with a full text were included in the review. Selection criteria Randomised controlled trials (RCTs) were included with adult participants (mean of 18-64.99 years) of all race/ethnic groups and gender on statin therapy with reported myopathic symptoms from an unknown cause. The intervention was in the form of a pure oral supplement of CoQ10 irrespective of dose, duration and frequency, and the control in the form of a placebo, a similar antioxidant, or no intervention. Outcomes included the severity of myopathic symptoms, levels of plasma creatine kinase (U/L), intramuscular CoQ10 (μmol/kg) and plasma CoQ10 (μmol/L), as well as adverse effects of CoQ10. Data collection and analysis The principle investigator and one independent reviewer selected the studies, extracted data and assessed for risk of bias using the Cochrane Collaboration‘s tool for assessing risk of bias. Authors of relevant clinical trials were contacted for additional information. Results Two RCTs were included in the review, totaling 76 participants. A meta-analysis could not be performed, thus the review is narrative. There were an insufficient number of RCTs to confirm whether routine supplementation of CoQ10 improves statin-induced myopathic symptoms. Conclusions More and larger RCTs are required to determine the efficacy of CoQ10 supplementation in statin-induced myopathy. Consensus needs to be reached regarding the definition and measurement instrument/s of myopathy so that results of future studies can easily be compared and synthesized.
AFRIKAANSE OPSOMMING: Agtergrond Statiene is medikasie bekend vir die effektiewe behandeling van hipercholesterolemie. Statien-geïnduseerde miopatie is egter 'n newe-effek wat voorkom in tot 15% van gebruikers, wat 'n vermindering in die voorgeskrewe dosis of staking van die medikasie tot gevolg het. Die presiese meganisme van statien-geïnduseerde miopatie is onbekend, maar die potensiaal van Koënsiem Q10 (CoQ10) is geïdentifiseer as 'n moontlike behandeling aangesien menslike plasma CoQ10 vlakke verlaag na die gebruik van statiene en as gevolg van die rol van CoQ10 in spierfunksie. Doelwitte Hierdie sistematiese literatuuroorsig het die effek van CoQ10 supplementasie bepaal op: die graad van statien-geïnduseerde miopatiese simptome, plasma kreatien kinase vlakke, intra-muskulêre en plasma CoQ10 vlakke, asook die teenwoordigheid van enige newe-effekte van CoQ10 supplementasie soos abdominale pyn, naarheid en braking of hoofpyne. Soektogstrategie Twee soektogte vir studies is uitgevoer in The Cochrane Central Register of Controlled Trials (ontstaan tot Maart 2011 en ontstaan tot November 2011), MEDLINE (ontstaan tot Maart 2011 en ontstaan tot November 2011), Web of Science (ontstaan tot Maart 2011 en ontstaan tot November 2011), Science Direct (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012), Wiley Online Library (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012), Springerlink (ontstaan tot April 2011 en ontstaan tot Februarie 2012), EBSCOhost [Academic Search Premier en CAB abstracts (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012), CINAHL (ontstaan tot Maart 2011 en ontstaan tot November 2011)], Scopus (ontstaan tot Maart 2011 en ontstaan tot November 2011) en Google Scholar (ontstaan tot Maart 2011 en ontstaan tot Februarie 2012). Verwysingslyste van artikels is ook met die hand nagegaan vir relevante kliniese proewe. Slegs kliniese proewe waarvan die volteks beskikbaar was, is ingesluit in die oorsig. Seleksiekriteria Ewekansige gekontroleerde proewe (EGP) is ingesluit met volwasse deelnemers (gemiddeld 18-64.99 jaar) van alle rasse/etniese groepe en geslag op statien-terapie met gerapporteerde miopatie simptome van onbekende oorsaak. Die intervensie was 'n suiwer orale supplement van CoQ10 ongeag die dosis, duurte en frekwensie, en die kontrole 'n plasebo, soortgelyke antioksidant, of geen intervensie. Uitkomste het ingesluit: die graad van miopatie simptome, vlakke van plasma kreatien kinase (U/L), intra-muskulêre CoQ10 (μmol/kg) en plasma CoQ10 (μmol/L), sowel as newe-effekte van CoQ10. Dataversameling en -analise Die hoof ondersoeker en een onafhanklike hersiener het die seleksie van studies en data-ekstraksie onderneem en die risiko vir sydigheid geassesseer deur gebruik te maak van die Cochrane Collaboration’s tool for assessing risk of bias. Outeurs van relevante kliniese proewe is geraadpleeg vir addisionele inligting Resultate Twee EGP is ingesluit in die oorsig met 'n totaal van 76 deelnemers. 'n Meta-analise kon nie uitgevoer word nie, dus is die oorsig beskrywend. Daar was te min EGP om te bewys dat roetine supplementasie van CoQ10 statien-geïnduseerde miopatiese simptome verbeter. Gevolgtrekkings Meer en groter EGP is nodig om die effektiwiteit van CoQ10 supplementasie in statien-geïnduseerde miopatie te bepaal. Konsensus moet bereik word ten opsigte van die definisie en metingsinstrument/e van miopatie sodat die resultate van toekomstige studies makliker vergelyk en verwerk kan word.
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Slowik, Ewa [Verfasser]. "Synthesis, endogenous detection, and mitochondrial function of the hydroxy-substituted Coenzyme Q10 derivative HO-Q10 / Ewa Slowik". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2021. http://d-nb.info/1229916660/34.
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Duberley, K. E. "Neurometabolic implications of coenzyme Q10 deficiency : pathogenesis, detection and treatment". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1416289/.
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Disorders of Coenzyme Q10 (CoQ10) biosynthesis represent the most treatable subgroup of mitochondrial diseases. Neurological involvement is frequently observed in CoQ10 deficiency, typically presenting as cerebellar ataxia and/or seizures. The aetiology of the neurological presentation of CoQ10 deficiency has yet to be fully elucidated and therefore in order to investigate these phenomena we have established a neuronal cell model of CoQ10 deficiency by treatment of the neuronal SH-SY5Y cell line with Para-AminoBenzoic Acid (PABA). This neuronal cell model provides insights into the effects of CoQ10 deficiency on neuronal mitochondrial function and oxidative stress. A marginal decrease in CoQ10 status (76% residual CoQ10) appears to be sufficient to impair Electron Transport Chain (ETC) function and increase mitochondrial oxidative stress, highlighting the vulnerability of neurons to a small deficit in CoQ10 status. In contrast to CoQ10 deficient fibroblasts, a CoQ10 deficiency (46% residual CoQ10) in neuronal cells appears to result in reversal of Complex V activity. This phenomenon has not been reported in previous studies of CoQ10 deficiency and may be a unique characteristic of neuronal cells. This neuronal cell model was subsequently utilised in the evaluation of candidate therapies for neurological conditions associated with CoQ10 deficiency. The efficacy of CoQ10 supplementation and methylene blue (MB) treatment were evaluated. CoQ10 supplementation proved effective at preventing mitochondrial oxidative stress and partially restoring neuronal mitochondrial function. However ETC complex activities were still compromised, suggesting an explanation for the refractory nature of neurological CoQ10 deficiency to treatment. Muscle is considered the “gold standard” for CoQ10 quantification; however neurological CoQ10 deficiency does not always present with a significant decrease in muscle CoQ10 status, despite a genetic diagnosis of CoQ10 deficiency. Cerebrospinal Fluid (CSF) CoQ10 quantification offers a more direct measurement of cerebellar CoQ10 levels. A tandem mass spectrometry (MS/MS) method capable of quantifying nanomolar (nM) levels of CoQ10 was therefore developed. In conclusion this PhD thesis has been successful in expanding our understanding of the pathophysiology of neuronal CoQ10 deficiency and subsequently suggesting why neurological CoQ10 deficiency might be refractory to CoQ10 treatment. This thesis has also led to the development of a new technique for quantification of CSF CoQ10 concentration, opening up many possibilities for future studies and applications.
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Janabi, Batool. "Vetenskapliga belägg för de påstådda effekterna av Rogaine (minoxidil) och Q10 Active Nattkräm (coenzym Q10) : En litteraturstudie". Thesis, Umeå universitet, Kemiska institutionen, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-66488.
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Pasha, Rand. "The Role of Coenzyme Q10 in Statin Treated Zebrafish (Danio rerio)". Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31427.
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Atorvastatin (ATV) is a member of the statin family of pharmaceuticals sold as Lipitor™ by Pfizer Pharmaceuticals. Statins inhibit HMG-Coenzyme A reductase (HMG-CoAR), thus inhibiting the biosynthesis of cholesterol and other isoprenoid compounds including Coenzyme Q10 (CoQ10). This study evaluated the role of CoQ10 in preventing ATV-induced myotoxicity using the zebrafish Danio rerio as a model organism. ATV reduced spontaneous swimming, response to tactile stimuli, whole body enzyme activities (citrate synthase, cytochrome oxidase and lactate dehydrogenase) as well as increased pericardial sac edema in larvae. Transcript abundance of muscle atrophy markers (atrogen-1, murf) and the mitochondrial biogenesis marker (pgc-1α) were also altered. Additionally, acute toxicity of adult zebrafish resulted in no change in locomotor behaviour; however tissue enzyme activities and transcript abundance were altered. These findings demonstrate the protective effect of CoQ10 against larval ATV-meditated reduction in responses to tactile stimuli and enzyme activities suggesting CoQ10 does play a role in ATV-mediated toxicity.
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Kurniawan, Dede Indra. "Statin-induced myopathy and the benefit of oral administration of coenzyme Q10". Thesis, Curtin University, 2007. http://hdl.handle.net/20.500.11937/1014.
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Background. Muscle cramps are one of the adverse affects suffered by hypercholesterolemia patients who are treated with statins. Besides reducing cholesterol levels, statins also reduce coenzyme Q10 (CoQ10) blood levels. One of several hypotheses of pathophysiology for statin-induced muscle cramps is reduced level of CoQ10. Besides being a very important antioxidant, CoQ10 also functions as a transmembrane proton conductor and an electron carrier between NADH and succinate dehydrogenases and the cytochrome system, which is needed for phosphorylation of ADP into ATP. Therefore, a decrease in the CoQ10 tissue levels, as reflected in its reduced blood levels, may contribute to the muscle function impairment. Researchers have proven that statins, drugs used to lower cholesterol, are able to reduce CoQ10 blood levels.Null Hypothesis. The administration of CoQ10 will have no effect on the frequency, severity and/or duration of muscle cramps amongst statin users.Aims. This study aimed to assess factors that might influence the development of statininduced myopathy manifested as muscle cramps, including the respondent’s age and sex; the dose and duration of their statin therapy; muscle symptoms (nature, duration and whether or not they have changed with statin use); other medicines consumed; and, other diseases suffered and to investigate the efficacy of oral CoQ10 supplements in reducing muscle cramps in statin users and non-users.Methods. The Study was comprised of two phases: Phase 1 the Muscle Adverse Effect Survey and Phase 2 the Coenzyme Q10 for Muscle Cramps Study. Data collection for Phase 1 took place from January 2006 to April 2006 in 45 community pharmacies throughout Western Australia. The second phase of the study, the clinical trial, took place through School of Pharmacy, Curtin University of Technology, from May 2006 to December 2006.Results. In the first phase of the study, the Muscle Adverse Effect Survey, it was found that the prevalence of myopathy amongst statin users was 22.3% (205/920). Amongst the respondents with muscle symptoms, 73/205 (35.6%) reported their muscle symptoms had worsened on using statins. Assuming non-respondents did not suffer from muscle problems reduced the overall incidence of potential statin-induced myopathy to 73/920 or 7.93%. It was found that atorvastatin was the most commonly prescribed statin (59.3%), followed by simvastatin (29.8%), then pravastatin (10.4%) and fluvastatin (0.6%). Despite the high use of atorvastatin, the incidence rate of myopathy by atorvastatin users was found to be similar with other statins. The most common muscle symptoms were night cramps (54.6%), muscle aching (52.7%), and fatigue (49.3%), while the most commonly affected area of the body was the calves (62%).Statistical analysis with multiple logistic regression showed increasing age, heart failure and the use of cortisone-like drugs increased the risk of muscle symptoms among statin users. It was found that, for every 1-year increase in age, the odds of suffering from muscle symptoms increased 1.039 (95% CI 1.019 – 1.061). Furthermore, taking cortisone-like medication increased the odds of suffering muscle symptoms 16.4 times (95% CI; 2.2 – 124.3), while participants with heart failure were 9.3 times (95% CI 1.2 – 73.2) more likely to develop muscle symptoms when prescribed statins.The second phase of the study, the Coenzyme Q10 for Muscle Cramps Study, was a single blind, placebo-controlled, cross over, 6-week evaluation of the benefits CoQ10 in reducing muscle cramps amongst statin users and non-users. It was found that on average, that statin users experienced a significant reduction in the severity of their muscle cramps, as indicated by lower average pain scores, during the period they were on CoQ10 (6.36 ± 0.75) compared with placebo (7.37 ± 0.85; p = 0.028). Furthermore, patients also experienced significantly shorter cramp duration when they were on CoQ10 (4.88 ± 0.84) than on placebo (5.84 ± 0.84; p = 0.001). In contrast, amongst non-statin users (who were used as controls), there were no significant differences between CoQ10 and placebo efficacy in all assessed variables.Conclusion. This study revealed that muscle symptoms were common among statin users, particularly those suffering from heart failure, taking corticosteroids, and increasing age. Furthermore, the administration of CoQ10 100 mg per day was safe and effective in reducing severity and duration of muscle cramps amongst statin users. However, these later findings need to be confirmed by larger, double blind, placebo controlled studies.
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Jansson, Helena. "Har Q10 någon effekt på smärtan vid statininducerad myopati/myalgi?" Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-72831.
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Sammanfattning Bakgrund:Koenzym Q10 (Q10) syntetiseras i kroppen och återfinns med de högsta koncentrationerna i hjärta, lever och immunförsvarets celler. Det har en viktig roll när det agerar transportör av elektroner i andningskedjan. Q10 har även antioxiderande egenskaper, stärker cellmembran och motverkar fettsyraoxidation i mitokondrien och cellmembran. Nyare studier visar att ett tillskott av Q10 även förbättrar symptomen vid kronisk hjärtsvikt och minskar kardiovaskulära händelser.Vid förhöjda blodfetter är det mest använda läkemedlet statiner. De hämmar kolesterolsyntesen i levern och de påverkar även syntesen av Q10 vilken också sker mevalonatvägen. En av de vanligaste biverkningarna vid statinbehandling är muskelbesvären myopati och myalgi. Studier visar att dåligt fungerande mitokondrier och reducering av Q10 i serum kan relateras till statinbehandling. Syfte:Syftet med detta arbete har varit att undersöka om ett tillskott av Q10 har någon reducerande effekt på smärtan vid statininducerad myopati (SIM). Metod:Denna litteraturstudie baserades på sex vetenskapliga artiklar sökta via PubMed. Studierna skulle vara randomiserade, dubbelblinda kliniska studier gjorda på människor. Av sökningens 10 träffar erhölls 6 artiklar vilka var relevanta för att besvara denna studiens frågeställning. Resultat:Resultatet visade att Q10 inte har någon större effekt på smärtan vid SIM. Endast 2 av 6 studier visar att Q10 har en god effekt. Slutsats: För att kunna dra slutsats om Q10 har effekt eller inte vid SIM behövs fler randomiserade placebokontrollerade studier med jämförbara grupper och fler antal deltagare.
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Bremer, Jan Daniel. "Die Wirkung von Ezetimib und/oder Simvastatin auf die Plasmakonzentration von Coenzym Q10 /". Bonn, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253855.
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Potgieter, Marnie. "Cellular effects of Coenzyme Q10 and resveratrol in the SJL/J dysferlinopathy mouse model". Thesis, University of Pretoria, 2010. http://hdl.handle.net/2263/24175.
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The muscular dystrophies (MDs) are genetic disorders of muscle degeneration due to mutations in genes that encode a wide variety of proteins. Dysferlinopathy encompasses a large variety of neuromuscular diseases characterized by the absence of dysferlin in skeletal muscle and an autosomal recessive mode of inheritance. Dysferlinopathy can manifest as limb girdle muscular dystrophy type 2B (LGMD 2B), Miyoshi myopathy (MM) or distal myopathy with anterior tibial onset (DMAT). The first symptoms usually appear during the second or third decade of life as clumsiness when running, fatigue when walking long distances and difficulty in climbing stairs. Progression of the disease eventually leads to a loss of ambulation. A deficit in membrane-repair machinery in dysferlinopathy suggested a direct role for dysferlin in the Ca2+-dependent membrane-repair process. Recently, dysferlin has also been implicated in the process of chemotaxis. Evidence exists that free radical mediated injury contributes to the pathogenesis of muscle necrosis in the muscular dystrophies. The imbalance of free radical synthesis and antioxidant capacity has been suggested to contribute to the necrotic process. It is therefore imperative to explore the effect of antioxidant supplementation in the MDs. The present study followed a novel approach in investigating the cellular effects afforded by the supplementation of the SJL/J mouse model for dysferlinopathy with the antioxidants, Coenzyme Q10 (CoQ10) and resveratrol. The study aimed to determine, at cellular level, the histopathology and ultrastructural changes in the SJL/J mouse model following a 90 day trial with antioxidant supplementation. In addition to studying the morphology, the study paid attention to nonspecific parameters. The study mainly focused on the histopathology and ultrastructural alterations in the SJLL/J mouse. In addition the oxidative stress index of the affected quadriceps muscle was determined. The outcome provides evidence that increased oxidative stress levels are present in the SJL/J mouse. Antioxidant supplementation with CoQ10 at 120mg/kg/day or a resveratrol/CoQ10 combination supplementation at 40 and 60mg/kg/day, decreased the levels of oxidative stress and dystrophic markers at a cellular level. In addition, increased physical strength was observed. This thesis provides evidence to create a new platform for combination therapeutic strategies.Thesis (PhD)--University of Pretoria, 2010.
Anatomy
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Molyneux, Sarah Lee. "Development of assays for coenzyme Q10 and vitamin K, and their application in clinical trials". Thesis, University of Canterbury. Chemistry, 2006. http://hdl.handle.net/10092/1328.
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This thesis describes the development of separate assays to measure coenzyme Q₁₀ (CoQ₁₀) and vitamin K. Coenzyme Q is essential for the mitochondrial electron transport chain, and vitamin K for the blood coagulation cascade. Vitamin K deficiency is associated with haemorrhagic disease of the new-born, and CoQ₁₀ deficiency with HMG-CoA-reductase inhibitor (statin) therapy and heart failure. Coenzyme Q and vitamin K are usually measured by HPLC, using electrochemical and ultraviolet, and electrochemical and fluorescence detection, respectively. For vitamin K1, the limit of detection achieved using fluorescence and electrochemical detection was 0.28 and 0.12 nmol/L, respectively. Sensitivity of fluorescence detection is improved by using protic solvents in the mobile phase, and platinum-black catalysed alcohol reduction. The lipophilicity and low endogenous concentrations of vitamin K1 hinder its measurement, and further work is required to produce a rapid, reliable and robust assay for its measurement in human plasma. The limits of detection achieved using fluorescence, ultraviolet and electrochemical detection to measure CoQ₁₀ were 29, 4.8, and 0.34 nmol/L, respectively. Plasma CoQ₁₀ is not stable during long term storage at -13 ℃, but at -80 ℃ it is stable for at least 18 months. The reference interval for plasma total CoQ₁₀ in the New Zealand population is 0.47 - 1.80 µmol/L. There is no clinical requirement for stratification of the reference interval according to gender. Coenzyme Q₁₀ in human plasma is homeostatically controlled, varying little over a two month interval in healthy young males. Coenzyme Q₁₀ supplements have significantly different bioavailability, with the median increase in plasma CoQ₁₀ ranging from 0.14 to 0.59 µmol/L for seven different supplement brands. There is a large inter-individual variation in CoQ₁₀ absorption, and hence plasma concentrations should be monitored during supplementation. A plateau in CoQ₁₀ absorption, from a single dose, at approximately 200 mg suggests that the maximum dose ingested at one time should be 200 mg or less. Q-Gel capsules containing 30 mg of CoQ₁₀ are twice as effective at raising blood CoQ₁₀ as 100 mg capsules. Plasma CoQ₁₀ in patients with chronic heart failure are significantly lowered by approximately 33% when these patients receive Atorvastatin for six weeks. The absolute decrease in CoQ₁₀ showed a significant correlation with worsening endothelial function (r = + 0.548, p = 0.011). Coenzyme Q₉ was shown to be present in human plasma with a reference interval of 8.8 - 47.0 nmol/L.
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Porter, David A. "The effect of oral coenzyme Q10 on the exercise tolerance of middle-aged, untrained men". Virtual Press, 1991. http://liblink.bsu.edu/uhtbin/catkey/776715.
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Dai, Yuk-ling Eunice, e 戴毓玲. "Effect of coenzyme Q10 supplementation on mitochondrial function and vascular function in patients with cardiovascular disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45152949.
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Adedeji, Adekunle. "The Combined Effects of Leptin and Coenzyme Q10 in Ameliorating Obesity- Induced Infertility in Female Rats". Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etd/3131.
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Infertility is one of the major problems of obesity. Studies have shown that administration of leptin reversed obesity-induced infertility in rats and mice. Coenzyme Q10 (CoQ10) is an antioxidant and also supplies the energy needed for ovulation and embryo development. We hypothesized that leptin when combined with CoQ10 could greatly improve obesity-induced infertility. The results showed a significant decrease in food intake, body weight, and the regular estrous cycle was restored after treatment with leptin+CoQ10. There was a significant increase (p10 significantly (p10 can improve fertility in obese infertile female rats. This study could provide a novel therapeutic strategy for the treatment of infertility and formulation of new drugs for the treatment of obesity-induced infertility in females.
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Adedeji, Adekunle, Effiong Ottukonyong, Jonathan M. Peterson e W. Andrew Clark. "The Combined Effects of Leptin And Coenzyme Q10 in Ameliorating Obesity-Induced Infertility in Female Rats". Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/2513.
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Infertility is one of the major complications of obesity. Studies have shown that administration of leptin modulated the expression of Β-catenin in the ovary and reversed obesity-induced infertility in rats. Coenzyme Q10 (CoQ10), an antioxidant, supplies the energy used for ovulation, oocyte and embryo development and prevents DNA damage that causes infertility. We hypothesized that leptin when combined with CoQ10 could greatly improve fertility. Twenty-one female Sprague-Dawley rats were used in this study and divided into five treatments groups. Group I rats was fed rat chow diet (RCD) while groups II to V were fed High-fat diet (HFD) for 14 weeks to induce infertility. Group 1 RCD and group II HFD control rats received 1 ml of saline intraperitoneally (i.p.) twice daily for 2 days, group III HFD rats received 1 ml of 100 µg of leptin i.p. twice daily for 2 days, group IV HFD rats received 10 mg/kg of CoQ10 i.p. for 2 weeks plus saline twice daily for 2 days. Group V HFD rats received 1 ml of 100 µg of leptin i.p. twice daily for 2 days plus 10 mg/kg of CoQ1o i.p. for 2 weeks. Estrous cycle was checked daily and food intake and body weight measured twice weekly before and after treatments. Fourteen days post treatment, all the animals were sacrificed. The blood and tissues were collected for analysis. The results show a significant decrease in food intake and body weight and regular estrous cycle restored in groups III and V rats. There was significant (p < 0.05) increase in spleen weight in groups IV and V. FSH level increased significantly (p < 0.05) in the leptin plus CoQ10 treated group while CoQ10 level was increased significantly (p < 0.05) in the leptin-treated group. Β-catenin expression was decreased in group IV and V, suggesting that Β-catenin expression may be downregulated by COQ10 administration. These results indicate that synergistic action of leptin and CoQ10 could delay the onset of obesity-induced infertility exhibited by the reduction of food intake and body weight. In conclusion, combinations of CoQ10 with leptin can improve fertility in obese infertile female rats and could provide a novel therapeutic strategy for the treatment of female infertility.
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Belhaj, Nabila. "Nano-émulsion naturelle de phospholipides marins, issus d’un complexe phospholipopeptidique provenant d’un procédé de valorisation de co-produits de saumon, et applications à la vectorisation de molécules faiblement biodisponibles". Thesis, Vandoeuvre-les-Nancy, INPL, 2011. http://www.theses.fr/2011INPL080N/document.
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Les bienfaits des acides gras oméga-3, essentiellement l’EPA (C20:5n-3) et le DHA (C22:6n-3) sont bien élucidés dans la littérature. Ils jouent en effet, un rôle essentiel dans la prévention de nombreuses maladies neurodégénératives et cardiovasculaires. Ces acides gras polyinsaturés à longue chaîne sont majoritairement retrouvés dans des sources d’origines marines. Dans ce contexte, nous nous sommes intéressés d’une part à l’effet du complexe phospholipopeptidique provenant de l’hydrolyse enzymatique des têtes de saumon, sur l’anxiété et le stress oxydant dans le cadre d’une étude comportementale effectuée sur un modèle murin. D’autre part, nous avons mis en place une approche de double vectorisation, sous formes de nanoémulsions, visant à augmenter la biodisponibilité de deux molécules hydrophobes et bioactives (coenzyme Q10 et curcumine) en utilisant les lipides totaux (phospholipides et triacylglycérols) du complexe phospholipopeptidique riche en EPA et en DHA. Les résultats de ce travail ont montré que le CPLP, sa fraction lipidique et peptidique ont un effet anxiolytique à une dose de 600 mg de CPLP/jour pendant 14 jours de traitement. Il a également été démontré dans cette étude que l’hydrolysat peptidique du CPLP diminue significativement, à double dose, le stress oxydant en baissant le niveau endogène des espèces réactives de l’oxygène (ROS) dans les neurones. D’autre part, pour une utilisation thérapeutique, la biodisponibilité du CoQ10 vectorisé à forte dose est améliorée jusqu’à 38 fois par la formulation huileuse composée de lipides polaires du CPLP. Concernant la supplémentation classique en CoQ10 en tant que complément alimentaire, la formulation émulsionnée présente une meilleure disponibilité à dose aigüe, avec une concentration plasmatique deux fois plus élevée que la formulation de référence. Malgré une activité anticancéreuse reconnue pour la curcumine, sa faible solubilité diminue sa biodisponibilité et limite de ce fait son utilisation. La formulation nanoémulsionnée de curcumine contribue à inhiber la prolifération de cellules cancéreuses (MCF7)The benefits of omega 3 fatty acids, mainly EPA (C20:5n-3) and DHA (C22:6n-3) are well understood in the literature. They indeed play an essential role in the prevention of many neurodegenerative and cardiovascular diseases. These polyunsaturated fatty acids are mostly found in marine sources. In this context, we were interested on the effects of phospholipopeptidic complex from the enzymatic hydrolysis of salmon heads on anxiety and oxidative stress using a behavioural study (mouse model). On the other hand, we have developed a double vectorization operating nanoemulsions, to increase the bioavailability of two hydrophobic and bioactive molecules (conenzyme Q10 and curcumine) by total lipids (phospholipids and triacylglycerols) from the phospholipopeptidic complex rich in EPA and DHA. The results of this study showed that the CPLP, its lipid and peptide fractions have an anxiolytic effect at a dose of 600 mg of CPLP / day for 14 days of treatment. It was also demonstrated that the peptide’s hydrolyzate ingested at double dose decreases significantly the oxidative stress by lowering the endogenous level of reactive oxygen species (ROS) in neurons. For therapeutic uses, the bioavailability of CoQ10 increased up to 38 times compared to referential formulation when verctorized at high dose in the oily formulation composed of CPLP’s total lipids. Regarding conventional CoQ10 supplementation as a dietary supplement, the emulsified formulation has a better availability at single dose, with plasma concentrations two times higher than the reference formulation. Although the anti-cancer activity of curcumine is highlighted, its low solubility and hence its low bioavailability, are factors limiting its use. The formulation of nanoemulsified curcumine allows a significant reduction in the proliferation of cancer cells (MCF7)
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Mischingerová, Monika. "Penetrační vlastnosti polymerních micel na bázi hydrofobizované kyseliny hyaluronové". Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2014. http://www.nusl.cz/ntk/nusl-217035.
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The aim of this thesis was to investigate the penetration features of the hydrofobized hyaluronic acid – based polymeric micelles using Nile red as carried tracer. Furthermore, to implement basic characterization of polymeric micelles for potential cosmetic applications using Coenzyme Q10 (CoQ10) as carried substance. It was found that the size of the polymeric micelles with carried CoQ10 did not exceed 100 nm. Applied delivery systems based on hydrophobic hyaluronic acid were suitable for potential topical application. Delivery systems with Nile Red as carried tracer demonstrated excellent penetration features. We assume that delivery systems with CoQ10 will exhibit similar penetration features. An issue has appeared whether the carrier breaks or proceeds along with NR to the skin. Moreover, another experiments have been designed which could also verify the penetration features of these systems.
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Bianchi, D. "'INVESTIGATION OF NEW EFFICIENT SYNTHESIS OF UBIQUINONES, MENAQUINONES DERIVATIVES AND UBIDECARENONE; COMPARISON OF PROBLEMS IN THE SYNTHETIC AND ANALYTICAL ASPECTS OF RESEARCH AND SCALING UP'". Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150052.
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An efficient and versatile synthetic method relating to Ubiquinone or Menaquinone derivatives compound is disclosed, leading to final compounds with high isomeric purity in good overall yields. The technologic transfer of the method allowed to solve industrial concern about the production; the present method has been scaled up, offering the possibility for the synthesis to compete with natural fermentative sources of such compounds.
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Licitra, Floriana. "Pathophysiological and molecular characterization of a mouse model of ARCA2, a recessive cerebellar ataxia associated to Coenzyme Q10 deficiency". Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ096/document.
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ARCA2 est une ataxie récessive qui se caractérise par une atrophie du cervelet et un léger déficit en coenzyme Q10. Des mutations dans le gène ADCK3 ont été récemment identifiées comme étant la cause d’ARCA2. ADCK3 code pour une kinase mitochondriale atypique, qui pourrait être impliquée dans la biosynthèse du coenzyme Q10. L’objectif de mon projet de thèse était d’élucider la physiopathologie d’ARCA2 en utilisant le modèle murin knockout pour Adck3. J’ai ainsi pu montrer que les souris Adck3-/- reproduisent de nombreux symptômes associés à ARCA2 et constituent un bon modèle pour étudier ARCA2. Au niveau du cervelet, les cellules de Purkinje sont spécifiquement touchées et présentent des anomalies morphologiques et fonctionnelles. Un léger défaut mitochondrial a été observé dans les muscles squelettiques des souris Adck3-/-. Enfin, une analyse transcriptomique de ces deux tissus a révélé des altérations de nombreuses voies, impliquant ADCK3 dans de nouveaux processus cellulairesARCA2 is a form of recessive ataxia characterized by a slow progression of the ataxic phenotype, cerebellar atrophy and mild deficit in Coenzyme Q10. ARCA2 was recently found associated with mutations in the ADCK3 gene that encodes a putativemitochondrial kinase homologous to the yeast Coq8 and the bacterial UbiB proteins, which are required for Coenzyme Q biosynthesis. In order to elucidate the pathophysiology of ARCA2, a constitutive knockout mouse for Adck3 was generated.Adck3-/- mice reproduce many ARCA2 symptoms such as slow progression of the ataxic phenotype and mild Coenzyme Q deficit, suggesting that Adck3-/- mice are a good model to study ARCA2. Strikingly, a morphological and functional impairmentwas found in cerebellar Adck3-/- Purkinje cells, whereas a mild mitochondrial defect was observed in the skeletal muscle of Adck3-/- mice. Interestingly, transcriptomic analyses revealed alteration in a number of molecular pathways implicating ADCK3in novel cellular processes
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Lagier-Tourenne, Clotilde Delphine. "Identification des gènes responsables du syndrome de marinesco-Sjögren et d'une forme d'ataxie avec déficient en coenzyme Q10". Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/LAGIER-TOURENNE_Clotilde_Delphine_2007.pdf.
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Par une stratégie de cartographie par homozygotie, nous avons identifié les gènes responsables de deux ataxies autosomiques récessives : le syndrome de Marinesco-Sjögren (MS) et une nouvelle forme d’ataxie associée à un déficit en coenzyme Q10 (CoQ). Le syndrome MS est une affection congénitale multisystémique avec notamment la présence d’une ataxie, d’une myopathie et d’une cataracte bilatérale. Nous avons localisé le gène en 5q31, et identifié en collaboration avec le Pr Lehesjoki des mutations dans le gène SIL1 codant pour un facteur d’échange nucléotidique d’une protéine chaperones HSP70. Puis, nous avons identifié des mutations d’ADCK3 dans une nouvelle forme d’ataxie. Les homologues d’ADCK3 chez E. Coli et S. Cerevisiae (respectivement ubiB et abc1/coq8) sont impliqués dans la biosynthèse du CoQ. Nous avons montré que les patients présentent un déficit en CoQ et qu’ADCK3 appartient à la super-famille des « kinases atypiques »By homozygosity mapping, we have identified the genes responsible for two autosomal recessive ataxia : Marinesco-Sjögren syndrome (MS) and a new form of recessive ataxia associated with coenzyme Q10 (CoQ) deficit. MS syndrome is a multisystemic disease with the association of an ataxia, a myopathy and bilateral cataracts. We have localized the gene on chromosome 5q31, and in collaboration with Pr Lehesjoki, we have identified mutations in the gene SIL1 encoding for a nucleotide exchange factor for an HSP70 molecular chaperonne. We have also identified mutations in the gene ADCK3 in a new form of ataxia. ADCK3 bacteria and yeast homologs (ubiB and abc1/coq8 respectively) are involved in CoQ biosynthesis. We have shown that the patients dysplay CoQ deficit and that ADCK3 belongs to the protein kinases-like superfamily
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Lagier-Tourenne, Clotilde Delphine Koenig Michel. "Identification des gènes responsables du syndrome de Marinesco-Sjögren et d'une forme d'ataxie avec déficit en Coenzyme Q10". Strasbourg : Université Louis Pasteur, 2007. http://eprints-scd-ulp.u-strasbg.fr:8080/961/01/LAGIER-TOURENNEC_2007.pdf.
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Franz, Karen Verfasser], e Hans-Konrad [Akademischer Betreuer] [Biesalski. "Unterstützung eines Gewichtsreduktionsprogramms durch Coenzym Q10 und Alpha-Liponsäure in micellierter wasserlöslicher Formulierung / Karen Franz. Betreuer: Hans-Konrad Biesalski". Hohenheim : Kommunikations-, Informations- und Medienzentrum der Universität Hohenheim, 2013. http://d-nb.info/1034572687/34.
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Fourie, Frans Jakobus. "The effect of exogenous coenzyme Q10 on its distribution and its role as protective agent against DNA damage / F.J. Fourie". Thesis, North-West University, 2003. http://hdl.handle.net/10394/386.
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Coenzyme Q10 (Q10) acts as an important in vivo anti-oxidant and has been widely
advocated to be a beneficial dietary adjuvant because elevated concentrations of Q10
should effect a higher energy production and anti-oxidant capacity, leading to lower
DNA damage and cell death. It remains controversial however, whether oral
administration of Q10 can significantly enhance its tissue levels and/or can modulate the
level of oxidative stress (DNA damage) in vivo.
We investigated whether oral administration of coenzyme Q10 (Q10) in mice could
increase the levels of its reduced form, Q10H2, in blood and in tissue (brain, liver and
heart) and determined the relationship between Q10H2 concentrations in the blood and
various tissues. These concentrations were correlated with cell DNA damage found in
blood and in brain, liver and heart tissue.
We also investigated if oral administration of Q10 could attenuate the neurotoxicity of 1-
methyl-4-phenyl-1,2,3,64etrahydropyridine (MPTP) in old mice, using damage to cell
DNA as the parameter.
In this study a method for assessing chemically and environmentally induced cell DNA
damage was developed, using the single cell gel electrophoresis (SCGE) assay and
compared these results with coenzyme Q concentrations in various tissue samples
obtained by using a validated HPLC analysis with electrochemical detection.
Four groups of one-year-old C57BL/6 mice received a standard diet or a diet
supplemented with Q10 (200mg/kg/day) for six weeks. After four weeks, one group that
had received the standard diet and one group that had received the Q10 supplemented
diet were treated additionally with one dosage of MPTP (40mg/kg).
The results showed that the Q10H2 as well as the Q9H2 concentrations were elevated in
the plasma, brain, heart and liver of those groups receiving Q10 and Q10 + MPTP. This
observation, as well as the phenomenon that the Q9H2 levels were higher than the
Q10H2 levels in the controls indicated that Q9 is the predominant Q homologue in mice
and that oral intake of Q10 increased the levels of both Q9H2 and Q10H2 in tissue and
blood.
The heart, brain and liver cells exhibited significantly higher DNA damage in the groups
treated with MPTP. The group receiving MPTP plus Q10 displayed less DNA damage
than the MPTP group indicating that Q10 most likely act as an ameliorating factor for
MPTP neurotoxicity. The blood samples before and after treatment in contrast, showed
very little difference in DNA damage. This might be explained by the fact that blood
cells regenerate much faster than other tissue.
Our findings indicate that levels of Q10 and Q9 can be increased in tissue by long-term
supplementation with Q10 and that Q10 could attenuate/prevent DNA damage in various
cells. This suggests that Q10 may be useful in disorders where there is impaired activity
of complex I, which might lead to DNA damage of the cell, such as Parkinson's disease.Thesis (M.Sc.)--North-West University, Potchefstroom Campus, 2004.
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Clement, Amy Marie. "The Antioxidant Defense Network: Synergistic Combinations to Prevent Oxidative Damage". BYU ScholarsArchive, 2008. https://scholarsarchive.byu.edu/etd/1549.
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One of the matchless ironies of the human body is its requirement for the highly reactive oxygen molecule, which has been clearly implicated in many diseases and the aging processes. Oxidants produced by metabolic processes damage cells by starting chemical chain reactions including oxidation of DNA and proteins as well as lipid peroxidation. Damage to DNA can cause mutations and lead to cancer if not reversed by DNA repair mechanisms. Damage to proteins causes enzyme inhibition, denaturation and protein degradation. Lipid peroxidation can cause cell lysis as well as creating mutagenic and carcinogenic by-products. The human body contains antioxidants and enzymes that together work to prevent oxidative damage to cellular components. By and large antioxidants either prevent these reactive oxygen species from being formed or remove them before they cause damage. There are many theories currently that tout the superior nature of diverse antioxidant combinations. One such theory is by Dr. Lester Packer of The University of California at Berkley. Dr. Packer puts forth the hypothesis that there is a superlative combination of five antioxidants that have the ability to "recharge" one another both in the blood plasma and intracellularly. This would result in a greater quality of antioxidant protection for an extended time. The current study evaluates Dr. Packer's theory of antioxidant combination from his book The Antioxidant Miracle. The decay rate of the antioxidants vitamin E, vitamin C, lipoic acid, glutathione, and coenzyme Q10 alone and in combination were determined using the ORAC (Oxygen Radical Absorbance Capacity) assay. The majority of the antioxidants retained activity for longer periods of time when tested alone, rather than in combination as Dr. Packer's theory would suggest. The assay was also preformed (using the same antioxidants and combinations) on oxidatively damaged Raji cancer cells. Cell viability and uptake of antioxidants into the cytoplasm were monitored. Finally, a variety of multivitamins were subjected to the ORAC assay and their antioxidant capacity compared to that of the "Packer Combination". The results suggest that multivitamins are superior antioxidants than the Packer ratio listed in The Antioxidant Miracle.
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Teuber, Sven Alexander. "Prävention der Kontrastmittelnephrophatie durch Ubiquinon (Coenzym Q10) bzw. durch die Kombination Ubiquinon/ Theophyllin bei Patienten mit eingeschränkter Nierenfunktion und Volumenüberladung". [S.l. : s.n.], 2007.
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Jaeg, Tiphaine. "Exploring the mitochondrial function in muscle and molecular dysregulation in cerebellum in a mouse model for ARCA2, a recessive ataxia with coenzyme Q10 deficiency". Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ082/document.
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ARCA2 est une ataxie autosomique récessive rare, caractérisée par une atrophie du cervelet et un léger déficit en Coenzyme Q10 (CoQ). La majorité des patients présentent des signes neurologiques supplémentaires comme l’épilepsie ou l’intolérance à l’exercice. La maladie est due à des mutations dans le gène COQ8A qui semble encoder une protéine kinase-like atypique, impliquée dans la biosynthèse du CoQ. Pour comprendre les mécanismes physiopathologiques, une souris Coq8a knock-out (KO) constitutif a été générée et récapitule les symptômes observés chez les patients. Le but de ce travail de thèse était de mieux comprendre certains aspects, notamment l’intolérance à l’exercice et l’ataxie. Malgré un déficit en CoQ dans les muscles, aucun défaut de respiration mitochondriale n’a été détecté dans un modèle cellulaire de muscle. Néanmoins, dans le cervelet, les niveaux de transcrits de 27 gènes sont dérégulés, précocement dans l’apparition de la pathologie chez les souris KO. Les voies métaboliques vont être explorées, ce qui devrait permettre de relier la fonction de COQ8A au taux de CoQ et aux symptômes observés chez les patientsARCA2, a rare form of recessive ataxia, is characterized by early onset progressive ataxia, cerebellar atrophy and a mild Coenzyme Q10 deficiency. Most of the patients show additional neurological signs such as epilepsy and exercise intolerance. Mutations in the COQ8A gene lead to ARCA2. COQ8A is suggested as being an unorthodox protein kinase like, with a regulatory role in CoQ biosynthesis, in mammals. To better understand ARCA2, a constitutive Coq8a knock-out (KO) mouse model was generated, which recapitulates most of the patient’s symptoms. Here we report the use of cellular models and the affected tissues to uncover the molecular signature of COQ8A loss and CoQ deficit. Despite CoQ deficit in the muscle, no mitochondrial bioenergetics defect was uncovered. In parallel, we have identified, by RT-qPCR, a key set of genes that are dysregulated in cerebellum, very early on in the pathology. We are currently investigating these pathways to uncover the link with COQ8A function. Altogether, our experiments will shed light on the early molecular events that lead to ARCA2 and may help draw a link between COQ8A function, CoQ pools and the symptoms observed in patients
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Alessandrini, Marco. "Evaluation of the effects of coenzyme Q10 and succinate in a rotenone-induced complex I deficient rat model / by Marco Alessandrini". Thesis, North-West University, 2006. http://hdl.handle.net/10394/491.
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Disorders of the mitochondrial respiratory chain have an incidence ranging from 1 in 2,000
to 1 in 5,000, with the most frequent of these cytopathies resulting from causative
alterations within mitochondrial complex I, the first enzyme of the respiratory chain. The
biochemical consequences of a complex I deficiency include, amongst others, failure to
oxidise reduced nicotinamide adenine dinucleotide (NADH), impairment of the Krebs
cycle, elevated blood lactate, lowered adenosine triphosphate (ATP) generation and an
increased production of reactive oxygen species (ROS).
The aim of the investigation was to evaluate the effects of CoQ10 and succinate in a
rotenone-induced animal model. Sprague Dawley rats were dosed with rotenone for a
period of 14 days via oesophageal intubation, resulting in the successful establishment of
a complex I deficient animal model. Upon optimisation of the rotenone concentration, rat
diets were supplemented with high concentrations of either coenzyme Q10 or succinate
for two days in an attempt to alleviate the biochemical manifestations of the rotenone induced
complex I deficiency. Five tissue types were collected and assayed for a total of
seven biochemical parameters, which enabled the establishment of a biochemical profile
of response for each of the tissue groups.
Data generated from the study revealed that rotenone, when dosed in high
concentrations, contributed to the alleviation of serum hydro peroxide levels. This result
was confirmed by the unexpected finding that rotenone itself harboured an antioxidant
capacity equivalent to that of Trolox, the vitamin E analogue generally used for the
determination of antioxidant capacity. It was therefore concluded that rotenone was not
an ideal inhibitor for the evaluation of complex I deficiency and ROS-related investigations
in an animal model. Since this compound is the most widely used inhibitor of complex I,
the data from the study affirms the use of alternative complex l inhibition strategies.
Finally, the data was suggestive of the fact that both coenzyme Q10 and succinate
exclusively improved isolated components of the biochemical profile. Results generated in
this study thus support current therapeutic intervention where patients receive a
combination of vitamins and cofactors as part of a management strategy for the
mitochondrial cytopathies.Thesis (Ph.D. (Biochemistry))--North-West University, Potchefstroom Campus, 2007.
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Schmelzer, Constance [Verfasser]. "Effects of coenzyme Q10 on gene expression and inflammation : results from in silico, in vitro and in vivo studies / Constance Schmelzer". Kiel : Universitätsbibliothek Kiel, 2010. http://d-nb.info/1019904569/34.
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Petersson, Kristina. "Har den lipidsänkande läkemedelsgruppen statiner en påverkan på neuropati?" Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-25699.
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Bakgrund: Av de kroniska sjukdomarna i världen orsakar hjärt-kärlsjukdomarna 17,5 miljoner dödsfall per år. Läkemedel som används för prevention mot hjärt-kärlsjukdomar är bl.a. statiner. Enligt Socialstyrelsen hämtade 455 716 patienter ut läkemedel från läkemedelsgruppen statiner från apoteken år 2011. Mellan åren 1988-2012 har Swedis (biverkningsdatabas) fått inrapporterat 24 biverkningsrapporter relaterat till statiner och neurologiska biverkningar som berör syftet i studien (perifer neuropati, polyneuropati, neuropati). Syfte: Studiens syfte var att sammanställa vetenskapliga publikationer rörande statiners direkta påverkan på perifera nervsystemet och eventuella förklaring till uppkomsten av neuropati. Resultat: De teorier som finns om hur statinbehandling kan ge neuropati säger att statiner, som ger en störd kolesterolsyntes, leder till rubbning i kolesterolrika neuronala membran. Även en minskad syntes av coenzymet ubiquinon ses, vilket påverkar mitokondriernas respiratoriska kedja och stör energiflödet till olika neuron. Statinbehandling har vidare visats öka risken att utveckla perifer neuropati. En ökad risk syns vid högre doser än rekommenderade samt vid långtidsbehandling. Statinbehandling vid diabetesrelaterad neuropati har däremot visats förbättra överledningshastigheten i motornerver med 5 % (P<0,05). Statinbehandling hos diabetes mellitus (DM) typ 2 patienter har visats ha en skyddande effekt från att utveckla perifer neuropati. Slutsats: Behandling med statiner ökar i takt med att vår tids folksjukdom, hjärt-kärlsjukdom, ökar. När behandling med statiner ökar, rapporteras samtidigt en bredare biverkningsprofil. Med statinbehandling ökar troligen risken för att utveckla neuropati speciellt vid användning av högre doser än rekommenderade samt vid långtidsbehandling. Däremot får statinbehandlade patienter med DM typ 2 en bättre nervöverledningsförmåga och ett skydd mot att utveckla perifer neuropati. En patientgrupp som därför troligen har god nytta av statinbehandling är DM typ 2-patienter. Att använda statiner till andra patientgrupper kanske istället kan leda till neuropati. Således kan skillnader mellan patientgrupper föreligga. Fler studier krävs dock för att bekräfta dessa resultat.Background: Cardiovascular disease is one of the chronic diseases that afflict the world with 17.5 million deaths per year, in particular coronary heart disease and stroke. The National Board in Sweden reported for 2011 that 464 847 patients collected drugs from the pharmacies that affect the serum lipid levels. The most collected drugs were statins standing for 455 716. The rare side effects (1/10 000) affecting the CNS (central nervous system) and the PNS (peripheral nervous system) were headache, parastesies, dizziness, peripheral neuropathy and polyneuropathy. Between the years of 1988 to 2012, the Swedis (a database of side effects) reported 258 adverse reactions related to statins and neurological side effects. Within the neurological side effect reports there were three groups related to the purpose in this study; peripheral neuropathy (2), polyneuropathy (10) and neuropathy (12). Objective: The purpose of this study was to collate scientific publications regarding the direct effects of the statins on the peripheral nervous system. It was also to present a possible explanation for the onset of neuropathy. Results: The theories concerning development of neuropathy with statin therapy includes a disturbed cholesterol synthesis, leading to disruption of cholesterol-rich neuronal membrane. Also, a decreased synthesis of ubiquinone coenzymes, which affect the electron transport of the mitochondrial respiratory chain, was shown. This in turn disturbs the flow production of energy (ATP) in the various neurons. Electrophysiological measurements were performed in many studies that showed changes in both sensory and motor nerves after treatment with statins. Statin therapy was shown to increase the risk of developing peripheral neuropathy. An increased risk was seen at higher doses than recommended, and in long term treatment. Statin treatment of diabetic neuropathy was shown to improve nerve conduction velocity in motor nerves with 5% (P <0.05). Statin therapy in type 2 DM (diabetes mellitus) patients was shown to have a protective effect from developing peripheral neuropathy. Larebs database in the Netherlands reports that the reporting odds ratios (ROR) were 3.7. The WHO reports that ROR was 2.86. Conclusion: Change of the nerve membrane in conjunction with a reduced cholesterol synthesis alters membrane composition thus function. A reduced cholesterol synthesis also seems to disturb the mitochondrial respiratory chain due to decreased levels of the coenzyme Q10, which in turn can cause neuropathy. Statin therapy increases the risk of developing neuropathy, especially when using higher than recommended doses and in long-term treatment. In contrast, statin-treated patients with DM type 2 got a better nerve conduction and protection against the development of peripheral neuropathy. A group of patients who probably therefore have good benefit of statin therapy is the DM type 2 patients. The use of statins to other groups of patients might instead cause neuropathy. More studies are needed to confirm the results. The frequency of reported adverse event reports involving statins and neuropathy is higher than other reported side effects.
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Wollstein, Christoph Michael [Verfasser], Mathias [Akademischer Betreuer] Winterhalter, Matias [Gutachter] Winterhalter, Jürgen [Gutachter] Fritz e Sergio S. [Gutachter] Funari. "The Location of Coenzyme Q10 in Phospholipid Membranes Made of POPE / Christoph Michael Wollstein ; Gutachter: Matias Winterhalter, Jürgen Fritz, Sérgio S. Funari ; Betreuer: Mathias Winterhalter". Bremen : IRC-Library, Information Resource Center der Jacobs University Bremen, 2015. http://d-nb.info/1135778515/34.
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