Tesis: "Oxidative Aging"

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AragÃo, Theresa Christine Filgueiras Russo. "Oxidative damages and ageing bean seeds Caupi". Universidade Federal do CearÃ, 2007. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=17178.

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FundaÃÃo Cearense de Apoio ao Desenvolvimento Cientifico e TecnolÃgico
The present study was carried out to elucidate the relationship between seed ageing and oxidative damage in two cowpea (Vigna unguiculata (L.) Walp.) cultivars, namely PitiÃba and PÃrola.The seeds were articially aged at 45 ÂC and 99% relative humidity until 72 h and daily harvested. Seed germination, electrolyte leakage, lipid and protein oxidation were evaluated. Moreover, changes in superoxide dismutase (SOD), ascorbate peroxidase (APX) and catalase (CAT) activity as their isoform pattern and CAT and APX mRNA expression were also investigated. Only in PÃrola seeds germinability was decreased whereas electrolyte leakage was increased with artificial ageing, indicating membrane damage. Moreover, PÃrola seeds presented higher lipid and protein oxidative damage than the PitiÃba ones. Total SOD activity was not altered by the treatment in both cultivars. Zymogram analysis reveled five different isoforms, designated SOD1 to SOD5 according to the eletrophoretic migration. No significant difference in the SOD isoenzyme pattern up to 72 h were detected. Specific inhibition with peroxide and cyanide showed SOD1 and SOD2 as SOD-Mn and SOD3, SOD4 and SOD5 as SOD-Cu/Zn isoforms. It was verified a cross-talk between CAT and APX activities through artificial ageing. At 72 h of treatment, CAT mRNA expression and activity increased in PitiÃba seeds and decreased in the PÃrola ones. Conversely, APX mRNA expression and activity showed an opposite pattern in the studied cultivars. Imunoblot analysis demostrated that no significant changes in CAT content were verified in PÃrola and PitiÃba seeds during induced aging. Thus, the CAT turnover did not necessarily involve coordinated mRNA synthesis, protein synthesis and protein degradation. In conclusion, lipid and protein oxidative damage were narrowly involved in seed aging in cowpea. PitiÃba seeds were more resistant to age-induced oxidative damage than that of PÃrola. PitiÃba seed resistance against aging were related to induced CAT expression and its activity, suggesting that this enzime play a role in oxidative damage protection.
O presente estudo foi desenvolvido na intenÃÃo de elucidar a relaÃÃo entre o envelhecimento de sementes e danos oxidativos em duas cultivares contrastantes de caupi (Vigna unguiculata (L.) Walp.), denominadas PitiÃba e PÃrola. As sementes foram artificialmente envelhecidas a 45 ÂC e 99% de umidade relativa atÃ 72 h e coletadas diariamente. GerminaÃÃo de sementes, vazamento de eletrÃlitos, oxidaÃÃo de lipÃdios e proteÃnas foram avaliados. AlÃm disso, alteraÃÃes em atividade de enzimas como dismutase de superÃxido (SOD), peroxidase de ascorbato (APX) e catalase (CAT) assim como o padrÃo de suas isoformas e expressÃo de RNAm de CAT e APX tambÃm foram investigados. Somente em sementes de PÃrola decresceu a germinabilidade enquanto que aumentou significativamente o vazamento de eletrÃlitos com o envelhecimento artificial, indicando danos de membrana. AlÃm disso, sementes de PÃrola apresentaram maiores danos oxidativos em lipÃdios e proteÃnas do que sementes de PitiÃba. A atividade total da SOD nÃo foi alterada durante o tratamento de sementes em ambas cultivares. AnÃlise de zimograma revelou cinco diferentes isoformas, designadas SOD1 a SOD5 de acordo com a migraÃÃo eletroforÃtica. NÃo houve diferenÃa significativa no padrÃo isoenzimÃtico de SOD durante as 72 h de tratamento. InibiÃÃo especÃfica com perÃxido de hidrogÃnio e cianeto revelou as isoformas SOD1 e SOD2 como SOD-Mn e SOD3, SOD4 e SOD5 com SOD Cu/Zn. Foi verificado um âcross-talkâ entre as atividades de CAT e APX durante o envelhecimento artificial. As 72 h de tratamento, a expressÃo de RNAm de CAT e sua atividade aumentaram em PitiÃba e diminuÃram em sementes de PÃrola. A expressÃo e a atividade de APX demonstrou um padrÃo oposto nas cultivares estudadas. AnÃlise de imunoblot demonstrou que nÃo houve alteraÃÃes significativas no conteÃdo de CAT em ambas as cultivares durante a induÃÃo do envelhecimento. Desse modo, o turnover de CAT nÃo envolve necessariamente a sÃntese coordenada de RNAm, sÃntese de proteÃna e degradaÃÃo de proteÃna. Em conclusÃo, danos oxidativos em lipÃdios e proteÃnas estÃo estreitamente envolvidos no envelhecimento de sementes de caupi. Sementes de PitiÃba sÃo mais resistentes aos danos oxidativos induzidos por envelhecimento do que sementes de PÃrola. A resistÃncia de sementes de PitiÃba contra o envelhecimento parece estar relacionada Ã induÃÃo da expressÃo e atividade de CAT, sugerindo que esta enzima realiza uma funÃÃo protetora contra danos oxidativos.

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2

Garg, Richa [Verfasser] y Elmar [Akademischer Betreuer] Heinzle. "Oxidative stress induced alterations during aging : quantifying the metabolic changes associated with aging and oxidative stress / Richa Garg ; Betreuer: Elmar Heinzle". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2017. http://d-nb.info/1140043331/34.

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3

Jervis, Kathryn. "Oxidative stress and aging of the male reproductive tract". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84264.

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The global demographic shift towards population aging will result in a dramatic increase in the numbers of elderly in the population. In order to cope with these changing demographics, it is imperative that we better understand aging and age-related pathologies. The reproductive tract provides an excellent system in which to study aging in that it is affected by aging, without compromising the overall health of the individual. In the Brown Norway rat model, the male reproductive tract (testis and epididymis) shows numerous signs of aging when other systems remain relatively unaffected by age, thus making this system ideal for studies on underlying causes of aging. One of the many theories proposed to account for the aging process is oxidative stress. Moreover, some of the changes that take place in the aging epididymis are suggestive of oxidative stress. In order to understand the contribution of oxidative stress to aging of the epididymis, we undertook global gene expression studies of the tissue in the young animal and then assessed how this gene expression was affected by age. We manipulated oxidative stress by caloric restriction and antioxidant (vitamin E) supplementation and deficiency. In characterizing the longitudinal gene expression in the young epididymis, we identified many genes never before reported in this tissue. We found that age profoundly affects gene expression in the epididymis and that the expression of oxidative stress related transcripts decreased, most dramatically in the distal (corpus and cauda epididymidis) regions of the tissue. Caloric restriction attenuated or reversed many of the gene expression changes that took place with age. The effect of caloric restriction was greatest for transcripts associated with protein synthesis and mitochondrial function. Finally, we found that long term antioxidant (vitamin E) deficiency resulted in increased expression of oxidative stress transcripts and exacerbated the effect

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4

Tsirklin, Liana. "Role of NADPH Oxidase in Oxidative Stress and Aging". Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/245082.

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As people age, their preferential adipose tissue stores tend to shift from subcutaneous to visceral, which could lead to diabetes, since visceral adipose tissue is insulin resistant. One of the proposed mechanisms for this shift is due to elevated levels of oxidative stress in adipose tissue cells due to aging, as a result of increased levels of NADPH oxidase (NOX). The goal of these experiments is to determine the existence and significance of this potential correlation. Visceral, subcutaneous, and stromal vascular adipose tissue samples from 18 week and 20 month old mice were probed for p47phox levels, a crucial component of NOX, and the levels of oxidative stress were also determined through a dinitrophenolhydrazine reaction in the OxyBlot analysis. In order to achieve these goals, electrophoresis gels were run, the gels were transferred through standard Western blot procedures, then probed with primary and secondary antibodies, and finally scanned and analyzed to determine differences in signal. As of yet, there have not been any statistically significant differences in oxidative stress levels determined in young and old mice, but further experiments will be conducted in order to validate these findings.

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5

Pournoman, Sara. "Oxidative Aging of Binders with High Recycled Asphalt Materials". Thesis, University of Nevada, Reno, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10282654.

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The objectives of this research effort focused on the oxidative aging of binders with high recycled asphalt materials. A coordinated program of forced-draft oven aging experiments was conducted on eleven sorts of binder blends including three different types of base binders from TX, NH, and NV, two different types of recycled material (RAP/RAS), and two different types of recycling agents (RA). Implementing the Fourier-Transform Infrared Spectroscopy (FT-IR) and Dynamic Shear Rheometer (DSR) isothermal frequency sweep tests, the oxidation kinetics and rheological performance were determined for the evaluation materials. Results indicated that the oxidative aging rates were influenced by the aging temperature, duration, base binder type, as well as the utilized asphalt modifier, i.e. recycled materials and RAs. It was also noted that the RAs reduced the overall stiffness in the investigated stages of oxidation. However, differential aging rates and hardening susceptibilities were observed between the RA and RAP/RAS additions to each of the three bases, noting that these differences were not consistent with the type of RAS, i.e. MWAS or TOAS. Additionally, the base binder aging properties due to the addition of the recycled material was highly influenced by the RA dosages within each blend.

Furthermore, the binder blend oxidative aging predictions at binder specific geographical location indicated that using the recycled materials along with the RAs at the optimum dosage, according to the proposed methodology, was able to restore the binder blend properties to the virgin binder.

The influences of the recycled material and RAs on the PG 64-28P base binder were also investigated through the binder PG grading and mortar testing. Consistent directions for the influence of the evaluation materials were observed within both procedures, suggesting the capability of the mortar procedure in characterizing the effects of RAP and RA materials on virgin binder without the use of chemical extraction.

The Uniaxial Thermal Stress and Strain Test (UTSST) was also conducted on the PMFC and RPMLC specimens of the NV field project to investigate the influence of the high recycled material and RAs on the asphalt mixtures. Through consideration of the thermo-viscoelastic properties, marked differences in the binder oxidation were noted between the experimental factors. Typically, decreases in the viscous response of the mixtures as well as increases in both the stiffness and brittle behavior were observed with aging and also inclusion of the recycled material. Although the addition of the RAs to the recycled mixtures indicated some extent of properties restoration, crack initiation and fracture were observed to occur in significantly warmer temperatures compared to the virgin mixture.

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6

Li, Ying Bo. "Anti-oxidative and pro-oxidative effects of curcuminoids on cellular senescence in aging and cancer". Thesis, University of Macau, 2011. http://umaclib3.umac.mo/record=b2492795.

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Lemon, Jennifer Rollo C. David. "Oxidative stress and aging processes in transgenic growth hormone mice". *McMaster only, 2005.

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8

Aragão, Theresa Christine Filgueiras Russo. "Danos oxidativos e o envelhecimento de sementes de feijão Caupi". reponame:Repositório Institucional da UFC, 2007. http://www.repositorio.ufc.br/handle/riufc/18805.

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ARAGÃO, Theresa Christine Filgueiras Russo. Danos oxidativos e o envelhecimento de sementes de feijão Caupi. 2007. 143 f. Tese (Doutorado em bioquímica)- Universidade Federal do Ceará, Fortaleza-CE, 2007.
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The present study was carried out to elucidate the relationship between seed ageing and oxidative damage in two cowpea (Vigna unguiculata (L.) Walp.) cultivars, namely Pitiúba and Pérola.The seeds were articially aged at 45 ºC and 99% relative humidity until 72 h and daily harvested. Seed germination, electrolyte leakage, lipid and protein oxidation were evaluated. Moreover, changes in superoxide dismutase (SOD), ascorbate peroxidase (APX) and catalase (CAT) activity as their isoform pattern and CAT and APX mRNA expression were also investigated. Only in Pérola seeds germinability was decreased whereas electrolyte leakage was increased with artificial ageing, indicating membrane damage. Moreover, Pérola seeds presented higher lipid and protein oxidative damage than the Pitiúba ones. Total SOD activity was not altered by the treatment in both cultivars. Zymogram analysis reveled five different isoforms, designated SOD1 to SOD5 according to the eletrophoretic migration. No significant difference in the SOD isoenzyme pattern up to 72 h were detected. Specific inhibition with peroxide and cyanide showed SOD1 and SOD2 as SOD-Mn and SOD3, SOD4 and SOD5 as SOD-Cu/Zn isoforms. It was verified a cross-talk between CAT and APX activities through artificial ageing. At 72 h of treatment, CAT mRNA expression and activity increased in Pitiúba seeds and decreased in the Pérola ones. Conversely, APX mRNA expression and activity showed an opposite pattern in the studied cultivars. Imunoblot analysis demostrated that no significant changes in CAT content were verified in Pérola and Pitiúba seeds during induced aging. Thus, the CAT turnover did not necessarily involve coordinated mRNA synthesis, protein synthesis and protein degradation. In conclusion, lipid and protein oxidative damage were narrowly involved in seed aging in cowpea. Pitiúba seeds were more resistant to age-induced oxidative damage than that of Pérola. Pitiúba seed resistance against aging were related to induced CAT expression and its activity, suggesting that this enzime play a role in oxidative damage protection.
O presente estudo foi desenvolvido na intenção de elucidar a relação entre o envelhecimento de sementes e danos oxidativos em duas cultivares contrastantes de caupi (Vigna unguiculata (L.) Walp.), denominadas Pitiúba e Pérola. As sementes foram artificialmente envelhecidas a 45 ºC e 99% de umidade relativa até 72 h e coletadas diariamente. Germinação de sementes, vazamento de eletrólitos, oxidação de lipídios e proteínas foram avaliados. Além disso, alterações em atividade de enzimas como dismutase de superóxido (SOD), peroxidase de ascorbato (APX) e catalase (CAT) assim como o padrão de suas isoformas e expressão de RNAm de CAT e APX também foram investigados. Somente em sementes de Pérola decresceu a germinabilidade enquanto que aumentou significativamente o vazamento de eletrólitos com o envelhecimento artificial, indicando danos de membrana. Além disso, sementes de Pérola apresentaram maiores danos oxidativos em lipídios e proteínas do que sementes de Pitiúba. A atividade total da SOD não foi alterada durante o tratamento de sementes em ambas cultivares. Análise de zimograma revelou cinco diferentes isoformas, designadas SOD1 a SOD5 de acordo com a migração eletroforética. Não houve diferença significativa no padrão isoenzimático de SOD durante as 72 h de tratamento. Inibição específica com peróxido de hidrogênio e cianeto revelou as isoformas SOD1 e SOD2 como SOD-Mn e SOD3, SOD4 e SOD5 com SOD Cu/Zn. Foi verificado um “cross-talk” entre as atividades de CAT e APX durante o envelhecimento artificial. As 72 h de tratamento, a expressão de RNAm de CAT e sua atividade aumentaram em Pitiúba e diminuíram em sementes de Pérola. A expressão e a atividade de APX demonstrou um padrão oposto nas cultivares estudadas. Análise de imunoblot demonstrou que não houve alterações significativas no conteúdo de CAT em ambas as cultivares durante a indução do envelhecimento. Desse modo, o turnover de CAT não envolve necessariamente a síntese coordenada de RNAm, síntese de proteína e degradação de proteína. Em conclusão, danos oxidativos em lipídios e proteínas estão estreitamente envolvidos no envelhecimento de sementes de caupi. Sementes de Pitiúba são mais resistentes aos danos oxidativos induzidos por envelhecimento do que sementes de Pérola. A resistência de sementes de Pitiúba contra o envelhecimento parece estar relacionada à indução da expressão e atividade de CAT, sugerindo que esta enzima realiza uma função protetora contra danos oxidativos.

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Luciano, Mateo Fedra Nicaury. "The role of chemokine (c-c motif) ligand 2 in inflammation, oxidative stress, aging and metabolism". Doctoral thesis, Universitat Rovira i Virgili, 2019. http://hdl.handle.net/10803/667564.

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El metabolisme i el sistema immunològic estan estretament relacionats i les seves interaccions juguen un paper important en l'homeòstasi sistèmica. L'activació, proliferació, diferenciació i polarització de les cèl·lules immunitàries representen un important estrès metabòlic, que pot comprometre el metabolisme cel·lular, l'homeòstasi i les necessitats energètiques. Aquestes condicions poden promoure l'estrès metabòlic crònic i les anomalies metabòliques en patologies no immunes. No obstant això, encara no queda clar com aquests canvis en el perfil immunològic afecten el metabolisme sistèmic. Cada vegada hi ha més proves de que les quimiocines exerceixen un paper crucial en tots aquests processos. Especialment, l'augment de la quimiocina C-C motif ligand 2 (CCL2) en malalties metabòliques suggereix la possibilitat que aquesta jugui un rol en la regulació del metabolisme. La pregunta clau és si l'augment de CCL2 és la causa o conseqüència del problema. Per aquesta raó, explorem l'efecte de la deficiència de CCL2 en el metabolisme de ratolins amb hiperlipèmia, esteatosis hepàtica i síndrome metabòlica. A més, es va investigar si aquest efecte podria estar condicionat per la dieta. Els resultats obtinguts es presenten en el primer estudi. Aquests resultats obren la porta a altres preguntes. Per exemple, la funció CCL2 va més enllà de la seva capacitat d'atraure cèl·lules immunitàries? Pot aquesta quimiocina afectar el metabolisme energètic? Per a respondre a aquestes preguntes, generem ratolins CCL2 cisgenic. Els resultats es presenten en l'estudi 2. En l'estudi 3 es va avaluar l'efecte de la sobre-expressió de CCL2 en un model de ratolí de la síndrome de progèria de Hutchinson-Gilford, un model d'envelliment accelerat. La cerca de dianes terapèutiques per al tractament de malalties metabòliques és un punt important en les recerques actuals. Els resultats d'aquesta tesi suggereixen que la CCL2 podria ser una diana terapèutica important en diferents malalties metabòliques.
El metabolismo y el sistema inmunológico están estrechamente relacionados y sus interacciones juegan un papel importante en la homeostasis sistémica. La activación, proliferación, diferenciación y polarización de las células inmunitarias representan un importante estrés metabólico, que puede comprometer el metabolismo celular, la homeostasis y las necesidades energéticas. Estas condiciones pueden promover el estrés metabólico crónico y las anomalías metabólicas en patologías no inmunes. Sin embargo, aún no está claro cómo estos cambios en el perfil inmunológico afectan al metabolismo sistémico. Cada vez hay más pruebas de que las quimiocinas desempeñan un papel crucial en todos estos procesos. Especialmente, el aumento de la quimiocina C-C motif ligand 2 (CCL2) en enfermedades metabólicas sugiere la posibilidad de que esta juegue un papel en la regulación del metabolismo. La pregunta clave es si el aumento de CCL2 es la causa o consecuencia del problema. Por esta razón, exploramos el efecto de la deficiencia de CCL2 en el metabolismo de ratones con hiperlipidemia, esteatosis hepática y síndrome metabólico. Además, se investigó si ese efecto podría estar condicionado por la dieta. Los resultados obtenidos se presentan en el primer estudio. Estos resultados abren la puerta a otras preguntas. Por ejemplo, ¿la función de CCL2 va más allá de su capacidad de atraer células inmunitarias? ¿Puede esta quimiocina afectar el metabolismo energético? Para responder a estas preguntas, generamos ratones CCL2 cisgénicos. Los resultados se presentan en el estudio 2. En el estudio 3 se evaluó el efecto de la sobreexpresión de CCL2 en un modelo de ratón del síndrome de progeria de Hutchinson-Gilford, un modelo de envejecimiento acelerado. La búsqueda de dianas terapéuticas para el tratamiento de enfermedades metabólicas es un punto importante en las investigaciones actuales. Los resultados de esta tesis sugieren que CCL2 podría ser una diana terapéutica importante en diferentes enfermedades metabólicas.
Metabolism and immune system are closely interconnected and their interactions play an important role in whole-body homeostasis. The activation, proliferation, differentiation and polarization of the immune cells represent significant metabolic stress, which can compromise the cellular metabolism, homeostasis and energetics requirements. These conditions can promote the chronic metabolic stress and metabolic abnormalities in non-immune pathologies. Nevertheless, how these changes in the immunological profile affect systemic metabolism are still not clear. Growing evidences support that chemokines play a crucial role in all these processes. Specially, the increase of chemokine C-C motif ligand 2 (CCL2) in metabolic diseases suggests the possibility of this chemokine to play a systemic role in the regulation of metabolism. The key question is if increase of CCL2 is the cause or consequence of the problem. For this reason, we explored the effect of CCL2 ablation in the metabolism of mice with a background of hyperlipidemia, hepatic steatosis and metabolic syndrome. In addition, we investigated whether that effect might be conditioned by diet. Obtained results are presented in the first study. These results open a brief to other questions. For example, does CCL2 function go further to its chemoattracting capacity? Can this chemokine affect the systemic energy metabolism? To answer these questions, we generated targeted CCL2 cisgenic mice, which overexpressed CCL2 in all tissues and results are presented in study 2. In study 3 we evaluated the effect of CCL2 overexpression in a mice model of Hutchinson-Gilford progeria syndrome, a model of accelerated aging. The finding of therapeutic targets for the treatment of metabolic diseases is an important point in current investigations in our research group. The conclusions of this thesis suggest that CCL2 could be an important therapeutic target in different metabolic diseases.

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10

Shao, Changxing. "OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION IN TRAUMATIC BRAIN INJURY IN AGING". UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_diss/533.

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Traumatic brain injury (TBI) is a prominent disease in developed countries, and age is an important factor in functional outcome. Although aged patients typically show diminished recovery compared to young patients, and have higher mortality and morbidity following TBI, the mechanism is not well understood. To date, there is no effective therapeutic for TBI. Previous studies indicate a secondary injury in TBI begins immediately after impact, and is likely the major contribution to delayed neuron dysfunction and loss. Studies also suggest mitochondrial dysfunction and increased free radical species (ROS) production following TBI may play a key role in the process. To evaluate oxidative damage following TBI, especially in aging, young (3 months), middle aged (12 months) and aged (22 months) Fisher-344 rats were subjected to a unilateral controlled cortical impact (CCI) injury, and tissue sparing, 4-hydroxynonenal (HNE) and acrolein levels, and antioxidant enzyme activities, and DNA oxidative damage were measured. In order to evaluate changes in mitochondria following TBI, mitochondrial protein levels were investigated using young adult animals. To evaluate a potential therapeutic for TBI, the effect of creatine on oxidative damage was evaluated. These studies show an age dependent increase of oxidative damage following TBI, demonstrated by increased levels of 4-HNE, acrolein and 8-hydroxyguanine. Middle aged and aged animals showed increased tissue loss compared to young animals 7 days post injury. Mitochondrial proteins involved in the respiratory chain, carrier proteins and channel proteins were significantly decreased 24 h post injury in ipsilateral cortex, but increased in both ipsilateral and contralateral hippocampus. To study potentially protective compounds in TBI, animals were fed with creatine two weeks before TBI and showed less oxidative damage and increased antioxidant capacity, which suggests creatine may be a potential drug for clinical treatment of TBI. The work described in this dissertation is the first to show increased oxidative damage and diminished antioxidant capacity in TBI in aging. The study of mitochondriafollowing TBI using quantitative proteomics is also the first time to show multiple mitochondrial proteins change following TBI. These data are also the first to show creatine can increase antioxidant defenses. These studies contribute to our understanding the mechanisms of secondary injury in TBI in aging.

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11

Morian, Nathan E. "Influence of mixture characteristics on the oxidative aging of asphalt binders". Thesis, University of Nevada, Reno, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3626103.

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The objective of this research effort focused on the evaluation of asphalt mixtures with respect to thermal cracking. Preliminary investigations soon indicated that a fundamental evaluation of thermal cracking was highly dependent upon the more complicated understanding of asphalt binder oxidation. The oxidation of asphalt binders within an asphalt mixture were understood to potentially be influenced by the mixture characteristics (i.e. air void levels, binder content, etc.) and aggregate properties (i.e. aggregate absorption, gradation, etc.). Therefore, this study was conducted in order to investigate and quantify the effects different aggregate sources and mixture properties may have on the oxidation and thermal cracking performance of asphalt mixtures.

The investigation specifically focused on quantifying the oxidation of the asphalt binder alone and as part of the asphalt mixture when subjected to isothermal oven aging. The oxidation parameters of pan-aged asphalt binders were quantified, according to the standard of practice in the industry. These parameters were then compared to extracted and recovered mixture-aged asphalt binders to examine the influence of the main aggregate and mixture factors on the binder oxidation. The study observed differences between the pan-aged and mixture-aged asphalt binders in terms of oxidation kinetics, rheological measures, and the combined effect represented as the hardening susceptibility.

Further evaluation of the binder oxidation based upon the dynamic modulus measures indicated marked influences of the mixture characteristics, the individual component materials, and the interactions between the investigated factors.

Differentiation of the experimental factors was further identified by the newly developed low-temperature evaluation method, Uniaxial Thermal Stress and Strain Test (UTSST). The UTSST provides a fundamental approach to characterize the thermo-viscoelastic properties of asphalt mixtures permitting the pragmatic evaluation of changes in the stiffness and overall behavior of mixtures as a function of oxidative aging. Five distinct stages in the UTSST modulus were identified as thermo-viscoelastic properties, which are identified as a function of temperature: viscous softening, viscous-glassy transition, glassy hardening, crack initiation, and fracture stages.

Through consideration of the thermo-viscoelastic properties, marked differences in the binder oxidation were noted between the experimental factors. Typically, decreases in the viscous response of the mixtures as well as increases in both the stiffness and brittle behavior were observed with aging. The evaluation method provides definitive measures to monitor multiple aspects of the performance of asphalt mixtures subjected to thermal loading.

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12

Lim, Christopher Y. (Christopher Yung-Ta). "Laboratory studies of the multiday oxidative aging of atmospheric organic aerosol". Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/121882.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Civil and Environmental Engineering, 2019
Cataloged from PDF version of thesis.
Includes bibliographical references.
Fine particulate matter (PM, or "aerosol") in the atmosphere affects the Earth's radiative balance and is one of the most important risk factors leading to premature mortality worldwide. Thus, understanding the processes that control the loading and chemical composition of PM in the atmosphere is key to understanding air quality and climate. However, the chemistry of organic aerosol (OA), which comprises a significant fraction of submicron atmospheric PM, is immensely complex due to the vast number of organic compounds in the atmosphere and their numerous reaction pathways. Laboratory experiments have generally focused on the initial formation of OA from volatile organic compounds (VOCs), but have neglected processes that can change the composition and loading of OA over longer timescales ("aging").
This thesis describes several laboratory studies that better constrain the effect of two important aging processes over timescales of several days, the oxidation of gas phase species to form secondary OA (condensation) and the reaction of gas phase radicals with organic molecules in the particle phase (heterogeneous oxidation). First, the oxidation of biomass burning emissions is studied by exposing particles and gases present in smoke to hydroxyl radicals (OH). Increases in organic aerosol mass are observed for all fuels burned, and the amount of OA formed is explained well by the extent of aging and the total concentration of measured organic gases. Second, the effect of particle morphology on the rate of heterogeneous oxidation is examined by comparing the oxidation of particles with thin organic coatings to the oxidation of pure organic particles.
Results show that morphology can have a strong impact on oxidation kinetics and that particles with high organic surface area to volume ratios can be rapidly oxidized. Third, the molecular products from the heterogeneous OH oxidation of a single model compound (squalane) are measured. Formation of a range of gas-phase oxygenated VOCs is observed, indicating the importance of fragmentation reactions that decrease OA mass, and providing insight into heterogeneous reaction mechanisms. The results from this work emphasize that the concentration and composition of OA can change dramatically over multiple days of atmospheric oxidation.
by Christopher Y. Lim.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Civil and Environmental Engineering

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Chen, Ying. "Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging". University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172086646.

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Davies, Stefan M. K. y n/a. "Oxidative damage to mitochondria on ageing in rats". University of Otago. Department of Biochemistry, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070403.111245.

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Ageing is a complex phenomenon, characterised by progressive loss of function, decreasing resistance to age-associated pathologies and stress, and increasing rates of mortality. The Free Radical Theory of Ageing implicates reactive oxygen and nitrogen species (ROS/RNS) generation as being integral to the ageing process, subjecting the organism to oxidative stress. Oxidative damage to biomolecules is suggested to be causative in the formation of ageing-associated phenotypes, dysregulation and dysfunction. Mitochondria are responsible for the production of the majority of ROS/RNS through normal functioning of the respiratory chain. Previous studies have reported increasing mitochondrial dysfunction with age, including oxidative damage to protein, lipid and DNA. Thus, mitochondrial dysfunction is considered by many to be central to the Free Radical Theory of Ageing. However, there are conflicting data on changes in mitochondrial and cellular function and damage on ageing. To investigate the role of mitochondrial protein oxidative damage in ageing, the heart, brain and liver of young (~ 2 month-old) and old (24 month-old) Wistar rats were fractionated into homogenate, cytosolic and mitochondrial fractions. Mitochondrial function was evaluated by measuring activity of the oxidative phosphorylation Complexes I-V, and correlating activity with quantitation of Complex subunits. The activities of the electron transport chain Complexes (I-IV) were largely unchanged on ageing, and no significant differences were seen in the protein levels of nuclear-encoded Complex I-IV subunits. There was a ~ 40% decrease in ATP synthase activity in heart and liver mitochondria from old rats as compared to young, but no change in the level of the Complex V nuclear-encoded subunit. These results suggest the decreased activity is due to modification of Complex V in heart and liver mitochondria on ageing, rather than changes in expression. Oxidative stress is a common cause of mitochondrial dysfunction, and is often accompanied by an increase in cellular antioxidant defences. Expression of the mitochondrial antioxidant enzyme, MnSOD, was found to be increased in the liver (+ 74%) and heart (+ 82%), but not brain, in old rats, suggesting oxidative stress in these organs on ageing in rats. To investigate generalised protein oxidative damage accumulation on ageing, whole tissue homogenate, cytosol and mitochondria were isolated from young and old heart, brain and liver. These fractions were assayed for three markers of protein oxidative damage: protein carbonyl content (a marker for generalised oxidative damage occurring via attack by many ROS/RNS), and ortho-tyrosine and meta-tyrosine accumulation (two markers specific for hydroxyl radical attack on phenylalanine). There were no consistent age-related changes in these biomarkers in any tissues, and no consistent significant differences between cytosolic and mitochondrial protein oxidative damage for any of the three tissues in the two age cohorts. Mitochondria were further subfractionated into membrane-enriched and matrix-enriched subfractions, but again, protein oxidative damage markers were largely unchanged on ageing. These results suggest that there is no common pattern of mitochondrial dysfunction during ageing in rats. Increased mitochondrial oxidative stress is a feature of ageing, but generalised protein oxidative damage is neither necessary nor sufficient for development of the ageing phenotype.

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15

Weir, Cameron 1981. "Aging and oxidative stress in epididymal spermatozoa of the Brown Norway rat". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101806.

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Aging is characterized by an imbalance in cellular redox status due to an increase in the production of reactive oxygen species (ROS) and a decreased activity of the cellular antioxidant defenses. Spermatozoa are highly susceptible to oxidative stress and hence this mechanism likely plays a causal role in the deficiencies associated with aging and male reproduction. The goal of this study was to determine the effect of age on antioxidant enzymatic activity, ROS production, and lipid peroxidation in spermatozoa along the epididymis of the Brown Norway rat. Aging significantly decreased glutathione peroxidase (Gpx)-1, Gpx4 and superoxide dismutase (SOD) activities and also significantly increased the production of hydrogen peroxide (H2O2) and superoxide (O2•-). Further, lipid peroxidation was found to be significantly increased in aged spermatozoa. These results indicate that aged spermatozoa are less capable of dealing with oxidative stress and provide a basis for the understanding of decreased spermatozoal quality in aging.

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16

Yi, Dong-Hui Chemistry Faculty of Science UNSW. "The Study of Biomarkers of Protein Oxidative Damage and Aging by Mass Spectrometry". Awarded by:University of New South Wales. School of Chemistry, 1999. http://handle.unsw.edu.au/1959.4/17636.

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The physiologically important free radicals, nitrogen monoxide and superoxide, can combine to form the reactive intermediate peroxynitrite. Peroxynitrite can react with proteins and their constituent amino acids, such as tyrosine, resulting in protein peroxidation, oxidation and nitration. The nitration of proteins, assessed by the analysis of 3-nitrotyrosine, is a proposed index of pathophysiological activity of peroxynitrite. The aim of the work was to investigate the reaction products between peroxynitrite and protein, develop an assay for 3-nitrotyrosine and measure its levels in biological samples. To study the amino acid products arising from the reaction of peroxynitrite and protein, both liquid chromatography (LC) and gas chromatography (GC) combined with mass spectrometry (MS) were adopted. Approaches to 3-nitrotyrosine assay development were first, to take advantage of the intrinsic sensitivity of electron capture negative ionization GC-MS. Secondly, to avoid possible artefactual problems associated with the derivatisation step in GC-MS, an assay for 3-nitrotyrosine based on combined LC-MS-MS was developed. When a selection of peptides was exposed to peroxynitrite under physiological conditions in vitro, the hydrolysis products showed that 3-nitrotyrosine was the major product. Detectable minor products were 3,5-dinitrotyrosine and DOPA. The GC-MS assay was found to be fraught with difficulty due to artefactual formation of 3-nitrotyrosine. In order to quantify and correct for artefact formation, this complication was approached by incorporating a second isotopomer. This method, however, was confounded by large errors that reduced the overall sensitivity. Either negative or zero levels of endogenous 3-nitrotyrosine were found in tested samples after correction for artefact formation. The LC-MS-MS assay was then used to analyse 3-nitrotyrosine levels in a range of biological samples, including human plasma from healthy volunteers, synovial fluid samples from arthritis patients and tissue extracts from a mouse model of amyotropic lateral sclerosis. In contrast to published data, 3-nitrotyrosine levels were found to be below the limit of detection (1 pg/????L, 10 pg o/c) for all samples - a result somewhat consistent with the negative GC-MS data. It is suggested that the high 3-nitrotyrosine levels previously reported in the literature might reflect artefactual generation of 3-nitrotyrosine and that other approaches to assessing pathophysiological nitration should be sought in future.

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17

Estery, Carmen M. "Mitochondrial uncoupling and remodelling during caloric restriction: Implications for oxidative stress and aging". Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28479.

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The 'uncoupling to survive' theory suggests that mitochondrial uncoupling protects cells from reactive oxygen species (ROS), thereby slowing aging. Caloric restriction (CR) mitigates aging; mechanisms may involve mitochondrial remodelling such that ROS production is decreased. It is unclear how uncoupling protein 3 (UCP3) in skeletal muscle is involved. Objective: To characterize effects of short-term 40% CR in wildtype (Wt) and UCP3 transgenic (UCP3 Tg) mice that possess uncoupled mitochondria. Hypothesis: In an uncoupled system, CR provides no further ROS protection. Approaches: Muscle mitochondrial and whole body assessments of UCP3's contribution to uncoupling and oxidative stress. Results: UCP3 Tg mice had lower body (P<0.001) and muscle weight (P<0.01), increased energy expenditure (P=0.12), similar body composition, increased proton leak (P<0.05), and decreased ROS production (P<0.05). In Wt mice, 1 mo CR mitigated ROS production (P<0.05), increased proton leak (P<0.05), decreased oxidative capacity (P<0.01), and increased UCP3 (P<0.05) protein levels. Such changes were not observed in UCP3 Tg mice. Overall, findings indicate that uncoupling in muscle does not reflect a pre-adaptation to CR. Rather, uncoupling delays the adaptive mitochondrial remodelling normally induced by short-term CR.

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18

Asano, Shinichi. "Aging influences multiple indices of oxidative stress in the heart of the Fischer 344/NNia x Brown Norway/BiNia rat". Huntington, WV : [Marshall University Libraries], 2007. http://www.marshall.edu/etd/descript.asp?ref=735.

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Theses (M.S.)--Marshall University, 2007.
Title from document title page. Includes abstract. Includes vitae. Document formatted into pages: contains ix, 81 pages including illustrations. Bibliography: p. 69-77.

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19

Hosseini, Seyed Mohsen. "Role of oxidative and energy metabolism in skin aging and UV-B induced carcinogenesis". Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0117/document.

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L’objectif de notre étude était de montrer le rôle du métabolisme oxydatif et énergétique au cours du vieillissement cutané et dans les cancers cutanés UVB-induits. Dans une première partie, nous avons cherché à établir un lien entre l'instabilité génétique, la production de ROS et l’altération métabolique dans le processus de vieillissement. Les résultats obtenus sur le modèle de souris XPC KO ont démontré qu’un excès de stress oxydatif dû à une sur activation du NOX1, couplé à des altérations métaboliques, jouaient un rôle prépondérant dans le vieillissement prématuré. L’application topique de notre nouvel inhibiteur de NOX, induisant l’inhibition de la production de ROS et ainsi l’apparition d’altération métabolique, a permis d’empêcher le vieillissement cutané prématuré chez les souris XPC KO. Nos résultats suggèrent que l’InhNOX peut être considéré comme une cible prometteuse dans la prévention du vieillissement prématuré et les maladies liées à NOX. Très peu d'informations sont disponibles sur la contribution de la reprogrammation du métabolisme énergétique dans l'initiation et la progression du cancer. Dans la deuxième partie de ma thèse, nous avons utilisé un modèle multi-étapes de cancer de la peau UVB-induits, nous permettant ainsi d’évaluer le rôle de la reprogrammation métabolique dans les différentes étapes de la cancérogenèse. Nous avons ensuite démontré que l'irradiation chronique à UVB entraînait une diminution de l’activité de la glycolyse, du cycle TCA et de la β-oxydation des acides gras, tandis que la synthèse d'ATP mitochondriale et une partie de la chaîne de transport d'électrons (CTE) étaient up-régulés. Nous avons montré que l’augmentation accrue de CTE été liée à la sur-activation des dihyroorotate déshydrogénase (DHODH). Alors que la diminution de l'activité DHODH ou ETC (chimiquement ou génétiquement) a conduit à une hypersensibilité à l'irradiation UVB. Nos résultats indiquent que la voie DHODH par l’induction de la synthèse d'ATP et de CTE joue un rôle majeur entre l'efficacité de réparation d'ADN et la reprogrammation métabolique au cours de la carcinogenèse UVB-induits
Objective of the present research study was investigating the role of oxidative and energy metabolism in skin aging and UVB-induced skin cancer. In the first part, we aimed to find the link between genetic instability, ROS generation and metabolism alteration in the process of aging. The obtained results on XPC KO mice model demonstrated that excess of oxidative stress in addition to alterations in energy metabolism due to over activation of NOX1 play a causative role in premature skin aging. Topical application of novel NOX inhibitor prevented the premature aging in XPC KO mice through inhibition of ROS generation and alteration of energy metabolism. Our results suggest that the InhNOX can be considered as a promising target in prevention of premature aging and NOX-associated diseases. Little information is available on the contribution of energy metabolism reprogramming in cancer initiation and promotion. To assess the role of metabolic reprogramming in different phases of carcinogenesis, in the second part of my thesis we employed a multistage model of ultraviolet B (UVB) radiation-induced skin cancer. We showed that chronic UVB irradiation results in decreased glycolysis, TCA cycle and fatty acid β-oxidation while at the same time mitochondrial ATP synthesis and a part of the electron transport chain (ETC) are upregulated. Increased ETC was further found to be related to the over-activation of dihyroorotate dehydrogenase (DHODH). Decreased activity of DHODH or ETC (chemically or genetically) led to hypersensitivity to UVB irradiation. Our results indicated that DHODH pathway through induction of ETC and ATP synthesis represents the relation between DNA repair efficiency and metabolism reprogramming during UVB-induced carcinogenesis

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20

Guzel, Aylin. "Photo-oxidative Degradation Of Abs Copolymer". Master's thesis, METU, 2008. http://etd.lib.metu.edu.tr/upload/12610895/index.pdf.

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ABSTRACT PHOTO-OXIDATIVE DEGRADATION OF ABS COPOLYMER Gü
zel, Aylin M.S., Department of Polymer Science and Technology Supervisor: Prof. Dr. Teoman Tinç
er Co-Supervisor: Prof. Dr. Cevdet Kaynak September 2009, 55 pages Acrylonitrile-butadiene-styrene (ABS) polymer is one of the most popular copolymer having an elastomeric butadiene phase dispersed in rigid amorphous styrene and semi-crystalline acrylonitrile. Due to double bonds in the polybutadiene phase, ABS copolymers are very sensitive to photo-oxidative degradation. Photo-oxidation of butadiene rubber phase results in the formation of chromorphores and these chromorphores act as initiators in photo-oxidative degradation and after a while ABS starts yellowing. In this work, the relationship between the UV light and the yellowing of ABS samples was also investigated with respect to time. In this study, pure, light stabilized and commercial ABS samples were aged under UV light. As the UV light intensity increased from 800 to 2800 &
#61549
W/cm2, yellowing of the samples were increased for pure ABS. This increase in yellowing of the samples was about 27 times higher compared to lower energy. In this study, UV stabilizers IRGANOX 1076 (sterically hindered phenolic antioxidant), IRGAFOS 168 (hydrolycally stable phosphite stabilizer) and TINUVIN P (hydroxyphenol benzotriazole) were used alone or in combination with each other. Pure ABS samples, commercial ABS samples and UV stabilized ABS samples were aged under the same UV light. UV aging degradation was followed by measuring the yellowness of the samples at certain time intervals. Yellowness of the samples was followed by using Coloreye XTH Spectrometer. Degradation in ABS, however, was followed by using FTIR with an increase in the peak area of carbonyl groups in the ABS matrix. Both color analysis and the FTIR analysis showed that combination of the IRGANOX 1076 and IRGAFOS 168 stabilizers gave the best stabilization. This revealed that combination of phenol and phosphate containing stabilizer is the most useful combination to prevent photo-oxidative degradation of ABS copolymer. Additionally, vegetable oil was applied to the surface of a new set of ABS samples and these samples were aged for 700 h. Yellowing tendency of these samples was compared with the yellowing tendency of ABS samples that are directly aged for 500 h. It was clearly observed that samples with oil smeared had more resistance to UV radiation with respect to others. This shows that oil acts protective layer to the UV light and oxygen and slow down the photo-oxidative degradation. Lastly some commercial ABS samples were compared to each other with respect to their yellowing tendency. Commercial ABS samples coded as K, L, A, B, C and D were aged under UV light at about 500 h. Sample A showed the best resistance against the yellowing among the other commercial ABS samples.

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21

Poon, Hung Fai. "REDOX PROTEOMICS IDENTIFICATION OF OXIDATIVELY MODIFIED PROTEINS AND THEIR PHARMACOLOGICAL MODULATION: INSIGHT INTO OXIDATIVE STRESS IN BRAIN AGING, AGE-RELATED COGNITIVE IMPAIRMENT". UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/287.

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The studies presented in this work were completed with the goal ofgaining greater insight into the roles of protein oxidation in brain aging and age-relatedcognitive impairment. Aging is associated with the impairment of physiological systemssuch as the central nervous system (CNS), homeostatic system, immune system, etc.Functional impairments of the CNS is associated with increased susceptibility to developmany neurodegenerative diseases such as Alzheimer's diseases (AD), Parkinson's disease(PD), and amyotrophic lateral sclerosis (ALS). One of the most noticeable functionalimpairments of the CNS is manifested by cognitive decline. In the past three decades, thefree radical theory of aging has gained relatively strong support in this area. Excessiveproduction reactive oxygen species (ROS) was demonstrated as a contributing factor inage-related memory and synaptic plasticity dysfunction. This dissertation use proteomicsto identify the proteins that are oxidatively modified and post-translationally altered inaged brain with cognitive impairment and normal aging brain.Ongoing research is being pursued for development of regime to preventoxidative damage by age-related oxidative stress. Among which are those that scavengefree radicals by antioxidants, i.e. ??-lipoic acid (LA), and protecting the brains byreducing production of neurotoxic substance, i.e. reducing production of amyloid ??(A??).Therefore, proteomics were also used to identify the alteration of specific proteins in agedbrain treated with LA and antisense oligonucleotides again amyloid protein precursor.This dissertation provides evidences that certain proteins are less oxidatively modifiedand post-translationally altered in cognitively impaired aged brain treated with LA andantisense oligonucleotides against the A?? region of amyloid precursor protein (APP)(AO).Together, the studies in this dissertation demonstrated that increased oxidativestress in brain play a significant role in age-related cognitive impairment. Moreover, suchincreased oxidative stress leads to specific protein oxidation in the brain of cognitiveimpaired subject, thereby leading to cognitive function impairment. Moreover, thefunctional alterations of the proteins identified by proteomics in this dissertation mayleads to impaired metabolism, decline antioxidant system, and damaged synapticcommunication. Ultimately, impairment of these processes lead to neuronal damages andcognitive decline. This dissertation also show that several of the up-regulated andoxidized proteins in the brains of normal aging mice identified are known to be oxidizedin neurodegenerative diseases as well, suggesting that the expression levels of certainproteins may increase as a compensatory response to oxidative stress. This compensationwould allow for the maintenance of proper molecular functions in normal aging brainsand protection against neurodegeneration.

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22

Opii, Wycliffe Omondi. "OXIDATIVE STRESS AND REDOX PROTEOMICS STUDIES IN MODELS OF NEURODEGENERATIVE DISORDERS: I. THE CANINE MODEL OF HUMAN AGING; II. INSIGHTS INTO SUCCESSFUL AGING; AND III. TRAUMATIC BRAIN INJURY". UKnowledge, 2006. http://uknowledge.uky.edu/gradschool_diss/299.

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The studies presented in this dissertation were conducted with the objective ofgaining greater understanding into the mechanisms of successful aging, the role ofmitochondria dysfunction in traumatic brain injury, and also on the mechanisms ofimproved learning and cognitive function in the aging.Aging is usually characterized by impairments in physiological functionsincreasing its susceptibility to dementia and neurodegenerative disorders. In thisdissertation, the mechanisms of dementia-free aging were investigated. The use of anantioxidant fortified diet and a program of behavioral enrichment in the canine model ofhuman aging was shown to result in a significant decrease in the levels of oxidativestress. A proteomic analysis of these brains also demonstrated a significant decrease inthe oxidative modification of key brain proteins and an increase in the expression levelsof other key brain proteins associated with energy metabolism and antioxidant systemswhich correlated with improved learning and memory.We show that following TBI key mitochondrial-related proteins undergoextensive oxidative modification, possibly contributing to the severe loss ofmitochondrial energetics and neuronal cell death previously observed in experimentalTBI.Taken together, these findings support the role of oxidative stress in thepathophysiology of aging and age-related neurodegenerative disorders and in CNS injury.These studies also show that antioxidants and a program of behavioral enrichmentprovide protection against oxidative stress-mediated cognitive impairments.

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23

Lopez-Cruzan, MariaLuisa (Marisa). "Role of caspase-2 in oxidative stress induced apoptosis : possible importance in aging : a dissertation /". San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1397904881&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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24

Poon, Hung Fai. "Redox proteomics identification of oxidatively modified proteins and their pharmacological modulation insights into oxidative stress in brain aging, mild cognitive impairment /". Lexington, Ky. : [University of Kentucky Libraries], 2005. http://lib.uky.edu/ETD/ukychem2005d00344/FaiPoon.pdf.

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Thesis (Ph. D.)--University of Kentucky, 2005.
Title from document title page (viewed on January 6, 2006). Document formatted into pages; contains: xviii, 554 p. : ill. Includes abstract and vita. Includes bibliographical references (p. 434-550).

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25

Furtado, Filho Orlando Vieira. "Efeitos crônicos não-térmicos das ondas eletromagnéticas não-ionizantes sobre o córtex cerebral e o fígado de ratos com diferentes idades". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/69713.

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O desenvolvimento tecnológico aumentou a exposição dos organismos às ondas eletromagnéticas (OEM). Dependendo das condições de exposição, este agente físico pode causar mudanças comportamentais, fisiológicas, celulares e moleculares. Neste nível de organização biológico, a literatura científica vem relacionando as OEM com o metabolismo das espécies reativas de oxigênio (ERO). Estas podem causar danos oxidativos a ácidos nucleicos, lipídios e proteínas. Entretanto, para se defender destas lesões, os sistemas biológicos apresentam defesas antioxidantes. O desequilíbrio entre oxidantes e antioxidantes ocasiona estresse oxidativo (EO), que pode ser observado em várias patologias neurodegenerativas e cardiovasculares, bem como nos processos de isquemiareperfusão e envelhecimento. Órgãos com altas taxas metabólicas e contendo muitos substratos oxidáveis, tais como o cérebro e fígado, são mais susceptíveis aos danos oxidativos. Sendo assim, o objetivo deste estudo foi verificar o efeito das OEM de UHF (ultra-alta-frequência) sobre os danos ao DNA, aos lipídios e às proteínas bem como sobre a expressão da catalase e o metabolismo de ácidos graxos insaturados (AGI) no fígado e córtex cerebral de ratos com diferentes idades (0, 6, 15 e 30 dias). Rattus norvergicus foram divididos em 2 grupos com 6 animais cada: ratos controles (RC) e ratos expostos (RE) às OEM com uma freqüência de 950 MHz, onda contínua, 1 W de potência, antena de polarização vertical, ½ hora por dia, durante 51 dias (21 da gestação + 30 de nascido). A taxa de absorção específica dos RE variou de 1,3 a 1,0 W/kg. Depois do período de exposição, os animais foram dissecados, o material foi congelado em nitrogênio líquido e armazenado no ultracongelador. Os danos ao DNA foram verificados pelo ensaio cometa alcalino; os danos oxidativos a proteínas, por PC (proteínas carboniladas); os danos oxidativos a lipídios, por TBARS (substâncias reativas com ácido tiobarbitúrico); a expressão da catalase foi verificada por immunoblotting; e a quantificação e a qualificação de ácidos graxos, por cromatografia gasosa. Nos resultados do fígado, os ratos 0 dia apresentaram menores níveis de TBARS e concentrações de AGI após exposição. Não houve diferença significativa de proteínas carboniladas em nenhuma das idades. Os danos ao DNA de RE de 15 e 30 dias foram significativamente diferentes. Os ratos com 0 dia expostos mostraram menor expressão de catalase. Nos resultados de córtex cerebral de 0 dia, não houve diferenças de TBARS e nem de PC no CCD (córtex cerebral direito) nem no CCE (córtex cerebral esquerdo). Os animais com 6 dias também não mostraram diferenças significativas de PC no CCE mas o CCD dos RE apresentaram maiores níveis de PC o que não foi observado em cometa. Os RE com 6 dias apresentaram menor concentração de glicose sangue total. Nossos resultados do fígado indicam que não há EO e nem genotoxicidade nos ratos com 0, 6, 15 dias de idade, mas há alteração na concentração de ácidos graxos polinsaturados de neonatos. Nos ratos com 30 dias, não há EO porém as OEM são genotóxicas. Os resultados do córtex cerebral de 0 e 6 dias indicam que não há lateralidade oxidativa e nem EO nos córtex. Entretanto, os maiores níveis de PC no CCD podem ser resultado de produtos finais de glicação avançada neste órgão. São necessários mais estudos para se entender os mecanismos das alterações em fígado de 0 e 30 dias bem como em CCD de animais com 6 dias de idade.
Technological development has increased the exposure of organisms to electromagnetic waves (EMW). Depending on the exposure conditions, this physical agent can cause behavioral changes, physiological, cellular and molecular. At this level of organization of animals, the scientific literature relating the OEM comes with the metabolism of reactive oxygen species (ROS). These can cause oxidative damage to nucleic acids, lipids and proteins. However, to protect these lesions, biological systems exhibit antioxidant defenses. The imbalance between oxidants and antioxidants cause oxidative stress (OS), which can be observed in several neurodegenerative disorders and cardiovascular disorders and in cases of ischemia-reperfusion injury, and aging. Organs with high metabolic rates and containing many oxidizable substrates such as the brain and liver, are more susceptible to oxidative damage. Therefore, the objective of this study was to investigate the effect of OEM UHF on damage to DNA, lipids and proteins as well as on catalase expression and metabolism of unsaturated fatty acids (UFA) in the liver and cerebral cortex of rats with different ages (0, 6, 15 and 30 days). Rattus norvegicus were divided into 2 groups of 6 animals each: control rats (CR) and exposed rats (ER) to the EMW with a frequency of 950 MHz, continuous wave, 1 W of power, vertical polarization antenna, ½ hour per day, for 51 days (21 days of gestation and 30 days of life outside the womb) . The specific absorption rate of ER ranged from 1.3 to 1.0 W / Kg. After the exposure period, the animals were dissected, material was frozen in liquid nitrogen and stored in ultrafreezer. The DNA damage were verified by alkaline comet assay, oxidative damage to proteins, for CP (protein carbonyls); oxidative damage to lipids by TBARS (thiobarbituric acid reactive substances), catalase expression was detected by immunoblotting, and quantification and qualification of fatty acids by gas chromatography. The results of the liver, 0 day rats had lower levels of TBARS concentrations and UFA after exposure. There was no difference in CP for any age. Damage to the DNA of ER with 15 and 30 days were different. Neonates (0 day) exposed showed lower expression of catalase. The results of the cerebral cortex of 0 day, there were no differences in TBARS and CP nor the RCC (right cerebral cortex) or the LCC (left cerebral cortex). The animals with 6 days also showed no differences in CP of LCC but the RCC of RE showed higher levels of CP which was not observed in comet. The ER with 6 days had lower total blood glucose concentration. Our results indicate that the liver no OS nor genotoxicity in rats with 0, 6, 15 days old but changed the concentration of polyunsaturated fatty acids in rats 0 day. In animals with 30 days no OS but the EMW are genotoxic. The results of the cerebral cortex of 0 day and 6 days indicated no oxidative lateral and OS in the cortex. However, the highest levels of the CP in RCC may be the result of advanced glycation end products in this organ. Further studies are needed to understand the mechanisms of changes in liver of 0 day and 30days as well as in animal RCC with 6 days old.

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Fukui, Hirokazu. "Mitochondrial Involvement in the Accumulation of Misfolded Proteins in Neurodegenerative Diseases". Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/41.

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Mitochondrial respiratory chain deficiency and increased oxidative stress have been closely associated with major age-associated neurodegenerative diseases. I hypothesized that mitochondrial oxidative phosphorylation defects or elevated oxidative stress, which could arise in a stochastic manner during our normal aging process, might modulate the formation of protein aggregates or production of misfolded proteins, contributing to the initiation of these diseases. To test this hypothesis, we (i) have developed and characterized mouse and cellular models of Alzheimer's and Huntington's diseases expressing aggregate-prone pathogenic proteins, beta-amyloid and mutant huntingtin (Chapters 1 and 2), (ii) have developed mouse models that exhibit neuron-specific defects in mitochondrial oxidative phosphorylation (Chapters 2 and 3), and (iii) have evaluated the alterations in the amount of aggregate loads upon genetic and pharmacological manipulations of mitochondrial oxidative phosphorylation activities (Chapters 1 and 2). The evaluation of the impacts of mitochondrial defects on the amount of huntingtin aggregates has revealed that a defect in complex III promotes the accumulation of huntingtin aggregates via the impairment of proteasome activity (Chapter 1). On the other hand, ablation of complex IV activity in a subset of postmitotic neurons revealed that complex IV deficiency does not promote either oxidative stress or the deposition of amyloid plaques in a mouse model of Alzheimer's disease, questioning the mitochondrial origin of Alzheimer's disease (Chapter 2). However, as shown previously, the tight correlation between oxidative stress and accumulation of amyloid plaques was found. Chapter 3 involved the generation of an improved mouse model, in which mitochondrial defects can be induced in a subset of forebrain neurons (cortex, hippocampus, and striatum) in a doxycycline-dependent manner. This system relies on the regulated expression of a mitochondria-targeted restriction enzyme, PstI, which digests mitochondrial DNA and thereby impairs the activity of oxidative phosphorylation. In conclusion, our studies highlighted the disease-specific complex pathways that may modulate the accumulation of misfolded proteins during aging. Future studies employing the newly-developed mouse model may reveal a contribution of age-associated global defects of oxidative phosphorylation to oxidative stress and neurodegenerative diseases.

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Domínguez, González Mayelín. "Daño oxidativo y regulación redox en el envejecimiento cerebral: vulnerabilidad regional". Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/565614.

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El presente trabajo exploró el proceso de envejecimiento cerebral humano considerando la vulnerabilidad regional específica en cuanto a eventos de daño oxidativo, respuesta antioxidante, metabolismo energético y moléculas implicadas en la inflamación. Se emplearon muestras de tejido post mortem de 12 regiones cerebrales (corteza frontal, corteza parietal, giro cingulado, corteza temporal, corteza entorrinal, hipocampo, tálamo, caudado, putamen, corteza visual, sustancia nigra y vermis) provenientes de 18 sujetos sanos de mediana y avanzada edad (grupos de edad). Mediante proteómica redox se identificaron 30 proteínas específicas susceptibles de ser lipoxidadas por NKT con patrones respecto a la edad y regionales específicos. Su vulnerabilidad a la lipoxidación se relacionó con patrones proteicos de localización, estructurales y funcionales. Además, el nivel global de NKT correlacionó con el nivel de oligómeros solubles, detectados por slot-blot, en las regiones con mayor aumento de la lipoxidación con la edad de proteínas específicas. Empleando Western-blot y densitometría se detectaron los niveles globales de marcadores de lipoxidación (NKT y MDA), glicoxidación (CEL y CML), defensas antioxidantes (SOD1, SOD2, CAT, GPX4, TRX1 y Nrf2), metabolismo energético (subunidades de los complejos mitocondriales: CI al CV, VDAC), metabolismo lipídico e inflamación (COX-2, CYP2J2 y vía NF-κB: p65, p50 e IκBα); y se exploraron sus diferencias con la edad en cada región comparando estadísticamente sus niveles entre grupos de edad. La lipoxidación proteica global presentó cambios con la edad específicos tanto para la región cerebral como el marcador estudiado. Los niveles globales de NKT se modificaron con la edad en pocas regiones cerebrales en contraste los de MDA, siendo este último el marcador que mostró más acusadamente cambios con la edad en el cerebro. Existió mayormente un aumento de la lipoxidación con la edad en las regiones en que variaron sus niveles (excepto NKT en tálamo y MDA en las cortezas temporal y entorrinal). Los niveles de las enzimas COX-2 y CYP2J2 presentaron variaciones con la edad y regionales en el cerebro, siendo el aumento de COX-2 característico del envejecimiento. Corteza frontal, corteza temporal e hipocampo podrían ser regiones particularmente susceptibles a alteraciones inflamatorias con la edad que involucren el metabolismo lipídico. Los niveles globales de glicoxidación proteica tendieron a aumentar durante el envejecimiento con patrones regionales específicos, a excepción de una disminución en hipocampo del CML. Varias regiones mostraron aumentos con la edad de glicoxidación no coincidentes con los de lipoxidación; durante el envejecimiento el daño a proteínas por glicoxidación podría ser más relevante en estas regiones que la lipoxidación. Se detectó una amplia modulación con la edad región-específica del nivel de enzimas antioxidantes, y discreta del factor transcripcional Nrf2. Los niveles de VDAC disminuyeron con la edad en tres regiones cerebrales (corteza frontal, corteza entorrinal y sustancia nigra), sugiriendo una disminución en el número de mitocondrias. En general, existió una amplia variación con la edad y regional en los niveles de los complejos mitocondriales del I al IV y poca en el CV; indicando que la regulación del nivel de los mismos (CI al IV) se modifica ampliamente en el cerebro humano con la edad. Se detectaron pocas variaciones con la edad y en cuanto a regiones cerebrales en los niveles de los componentes de la vía de respuesta NF-κB explorados. Giro cingulado, caudado y putamen resultaron las regiones en las que más se modificaron los componentes de esta vía con la edad. Además, el conjunto de datos permitió, mediante análisis bioinformático, establecer un perfil de vulnerabilidad regional con el envejecimiento en el cerebro que refleja en parte la tendencia a la neurodegeneración, apoyando la relevancia de los procesos redox en el envejecimiento y la susceptibilidad a la neurodegeneración.
The present work explored the process of human brain aging considering the specific regional vulnerability in terms of oxidative damage events, antioxidant response, energy metabolism and molecules involved in inflammation. Post mortem tissue samples from 12 brain regions (frontal cortex, parietal cortex, cingulate gyrus, temporal cortex, entorhinal cortex, hippocampus, thalamus, caudate, putamen, visual cortex, substantia nigra and vermis) were used, from 18 healthy subjects of middle and advanced age (age groups). By means of redox proteomics, specific proteins were identified as lipoxidized by NKT with particular age and regional patterns. Their vulnerability to lipoxidation was related to localization, structural and functional patterns. In addition, the overall level of NKT correlated with the level of soluble oligomers, detected by slot blot, in regions with high increase in the lipoxidation of specific proteins with age. By using Western blot and densitometry, the levels of lipoxidation (NKT and MDA), glycoxidation (CEL and CML), antioxidant defenses (SOD1, SOD2, CAT, GPX4, TRX1 and Nrf2), proteins involved in energy metabolism (subunits of mitochondrial complexes: CI to CV, VDAC) and lipid metabolism and inflammation (COX-2, CYP2J2 and NF-κB pathway: p65, p50 and IκBα) were explored in brain aging. In each brain region, their level modifications with age were tested by statistical comparison between age groups. The particular regional and age specific changes for these markers are reported and discussed throughout the work. In addition, the data set allowed to establish, by bioinformatic analysis, a regional vulnerability profile with aging in the brain which partly reflects the trend towards neurodegeneration, supporting the relevance of redox processes in brain aging and susceptibility to neurodegeneration.

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28

Vinayak, Anubhav. "Role of Oxidative Stress in Diabetes Mellitus". Youngstown State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1526905602340959.

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Son, Jyung Mean. "Age-associated metabolic reprogramming, oxidative stress response, and cancer progression". Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5856.

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Replicative and chronological lifespan are two different modes of cellular aging. Chronological lifespan is defined as the duration during which quiescent normal cells retain their capacity to re-enter the proliferative cycle. This study investigates whether changes in metabolism occur during aging of quiescent normal human fibroblasts (NHFs) and the mechanisms that regulate these changes. Bioenergetics measurements were performed in quiescent NHFs from younger (newborn, 3-d, 5-m, and 1-y) and older (58-y, 61-y, 63-y, 68-y, and 70-y) donors as well as NHFs from the same individual at different ages (29-y, 36-y, and 46-y). Results show significant changes in cellular metabolism during aging of quiescent NHFs: old NHFs exhibit significant decreases in glycolytic flux and lactate levels, and increases in oxygen consumption rate (OCR) and ATP levels compared to young NHFs. Results from Seahorse Mito Stress Test show that old NHFs with a lower Bioenergetic Health Index (BHI) are more prone to oxidative stress compared to young NHFs with a higher BHI. The increase in OCR in old NHFs is associated with a shift in mitochondrial dynamics more towards fusion. Genetic knock-down of mitofusin 1 (MFN1) and optic atrophy 1 (OPA1) in old NHFs decreased OCR and shifted metabolism more towards glycolysis. Downregulation of MFN1 and OPA1 also suppressed the radiation-induced increase in doubling time of NHFs. These results suggest that a metabolic shift from glycolysis in young to mitochondrial respiration in old NHFs occurs during the chronological lifespan, and MFN1 and OPA1 regulate this process. Age-associated metabolic reprogramming can also impact the age-related disease progression such as cancer. Recent evidence suggests a significant role of fibroblasts in pancreatic ductal adenocarcinoma (PDAC) stromal cellularity, metabolism, and therapy response. Considering PDAC being an age-related disease and a dismal 5-y survival of less than 9%, this study investigates whether stromal aging regulates PDAC progression. Results show that NHFs from older healthy individuals stimulate proliferation of PDAC cells compared to younger NHFs. Results from an in vivo study show that rate of tumor growth in xenografts of PDAC cells cultured with the old NHFs is significantly increased compared to the co-cultures of the young NHFs. In addition, decreased survival was also observed in mice carrying xenograft of co-culture of PDAC and the old NHFs compared to the young NHFs. Results from quantitative RT-PCR assays show that arachidonic acid lipoxygenase (ALOX12) expression decreased in PDAC, but increased in stromal fibroblasts in an age-dependent manner. Molecular inhibition of ALOX12 in the old NHFs suppressed PDAC proliferation in co-culture. These results show that aging of stromal fibroblasts aging promotes progression of PDAC, and identified ALOX12 and its metabolite 12-hydroxyeicosatetraenoic acid (12(S)-HETE) as critical regulators of PDAC proliferation. Taken together, findings from this project demonstrate that age-associated metabolic reprogramming of NHFs from glycolysis in young to mitochondrial respiration in old regulates fibroblasts-induced stimulation of proliferation of human PDAC. Importantly, results from this study are anticipated to contribute to the development of novel approaches targeting stromal aging for cancer prevention and therapy response.

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30

Sudama, Gita. "There are observable metabolic signature patterns in C. elegans specifically for different life stages grown with and without the added antioxidants Vitamin C and Vitamin E? /". Fairfax, VA : George Mason University, 2008. http://hdl.handle.net/1920/3088.

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Thesis (Ph.D.)--George Mason University, 2008.
Vita: p. 214. Thesis director: James D. Willett. Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Bioinformatics. Title from PDF t.p. (viewed July 7, 2008). Includes bibliographical references (p. 204-213). Also issued in print.

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31

Gangadharappa, Harish [Verfasser]. "Molecular events related to oxidative and nitrosative stress during brain aging, neurodegeneration and neurotrauma / Harish Gangadharappa". München : GRIN Verlag, 2020. http://d-nb.info/1205545492/34.

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Li, Mengjia Hsuan Grace. "Evaluation of oxidative behavior of polyolefin geosynthetics utilizing accelerated aging tests based on temperature and pressure /". Philadelphia, Pa. : Drexel University, 2005. http://dspace.library.drexel.edu/handle/1860/467.

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Feng, Jinliu 1974. "Mitochondrial respiratory transportation is the key determinant of aging in Caenorhabditis elegans". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32991.

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'The rate of living' hypothesis of aging speculates that the metabolic rate of a species ultimately determines its life expectancy. Using the nematode worm Caenorhabditis elegans as model system, mutation in twp-1 (t&barbelow;ime w&barbelow;arp) gene was found to significantly delay biological timing and remarkably increase mean and maximum life span. The rate of living in twp-1 is dramatically delayed in all the biological processes we tested, including rates of rhythmic adult behaviors, development, and reproduction. Oxygen consumption, which indicates metabolic rate of an organism, is reduced to approximately two-fold in twp-1 mutant. According to my study, twp-1 and dauer genes, daf-2 and daf-16, interact to determine biological timing and adult life span. twp-1 mutation prolongs life span in a way that is at least partially different from dauer formation mutants, whose longevity might due to their high resistance to stresses, especially oxidative stress. twp-1 gene is cloned and found to encode iron-sulfur protein (ISP) in complex III, which is the major site of mitochondrial superoxide radical production, of the mitochondrial respiratory chain. This suggests that twp-1 may live long because they produce less reactive oxygen species (ROS), and thus, result in less oxidative damage. mts-1 (mitochondrial twp-1 suppressor) mutation can fully or partially rescue most of the biological timing in twp-1 mutant, including both developmental and behavioral rates, but except life span. mts-1 encodes another subunit of complex III, cytochrome b, which normally interact with ISP during function. mts-1 might somehow restore the activity of complex III, and consequently, accelerate the rate of living. Paraquat, a herbicide that induces the formation of superoxide, was used to provide an acute oxidative stress to animals. twp-1; mts-1 was found to be highly resistant to paraquat, indicating that twp-1 animals are well capable of coping with oxidative stress. According to o

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34

Jacomini, André Mourão. "Exercício físico e estresse oxidativo: influência do nível de condicionamento físico na hipertensão arterial e na relação entre substâncias antioxidantes e oxidantes em idosos". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17152/tde-08102015-165014/.

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Introdução: A hipertensão arterial sistêmica (HAS) tem sido apontada como um dos principais fatores de risco para as doenças cardiovasculares, especialmente para a população idosa. O estresse oxidativo e o sedentarismo têm sido apontados como fatores etiológicos da HAS. Níveis elevados de estresse oxidativo são caracterizados pelo aumento na produção de espécies reativas de oxigênio, que tem forte afinidade com o óxido nítrico, o qual tem participação no processo de controle da pressão arterial. O exercício físico tem sido apontado para a regulação dessa relação. Objetivos: Investigar a relação existente entre as concentrações de óxido nítrico e a atividade pró e antioxidante e, se esta relação pode ser modulada por diferentes níveis de condicionamento físico; verificar se bons níveis de condicionamento físico contribui para um melhor controle dos valores de pressão arterial de idosos e sua influência no equilíbrio entre marcadores pró e antioxidantes de idosos. Método: Estudo transversal realizado em Bauru, SP, Brasil, com 161 idosos com idade média de 66,94 (6,83) anos. As variáveis estudadas foram: a aptidão física avaliada por meio da determinação indireta do VO2max e da bateria de testes motores proposta pela American Alliance for Health, Physical Education, Recreation and Dance (AAHPERD) para o cálculo do índice de aptidão funcional geral (IAFG); variáveis antropométricas relacionadas aos fatores de risco para o desenvolvimento de doenças cardiovasculares; medida de biomarcadores de estresse oxidativo (superóxido dismutase, glutationa peroxidase, substâncias reativas ao ácido tiobarbitúrico e medida de proteínas carboniladas) e substâncias vasodilatadoras ( nitrito, nitrato);O tratamento dos dados deu-se por estatística descritiva e o coeficiente de correlação de Pearson foi realizado para detectar correlação entre as variáveis. ANOVA de um fator com post-hoc de Tukey foi utilizado para detectar diferenças entre os grupos (p<0.05). O IAFG foi considerado como variável independente. Resultados: Os resultados gerais do presente estudo mostraram que bons níveis de condicionamento físico foram relacionados com menores níveis de atividade pró-oxidantes, maiores níveis de atividade antioxidante e maior concentração de substâncias vasodilatadoras. Essa combinação pode ser responsável por menores níveis de pressão arterial em indivíduos com melhor condicionamento físico.
Background: Systemic arterial hypertension (SAH) has been appointed as one of the main risk factors for cardiovascular disease, especially for elderly population. Oxidative stress and sedentary lifestyles have been suggested as etiological factors SAH. High levels of oxidative stress are characterized by increased production of reactive oxygen species, which has strong affinity with nitric oxide, which participates in blood pressure control process. Exercise has been pointed to regulate this relationship. Objectives: Investigate the relationship between nitric oxide concentrations and the pro and antioxidant activity, and if this relationship can be modulated by different physical fitness levels; verify if good physical fitness levels contributes to a better control of blood pressure values of the elderly and its influence on the balance between pro and antioxidant markers of elderly. Methods: Cross-sectional study performed in Bauru, SP, Brazil, with 161 elderly with an average age of 66,94 (6,83) years old. The variables studied were: physical fitness was evaluated by indirect determination of maximal oxygen uptake and by Functional Fitness Battery Test proposed by American Alliance for Health, Physical Education, Recreation and Dance (AAHPERD) to determine the general fitness functional index (GFFI); anthropometric variables related to risk factors for the development of cardiovascular disease; measuring of biomarkers of oxidative stress (superoxide dismutase, glutathione peroxidase, thiobarbituric acid reactive substances and measuring protein carbonyls) and vasodilator substances (nitrite and nitrate); Descriptive statistics was calculated and Pearsons correlation coefficient was performed to detect correlation among variables. One-way ANOVA with Tukey post-hoc test was performed to assess statistically significant differences between groups (p<0.05). The GFFI was considered as an independent variable. Results: The general results of this study showed that good levels of physical fitness were related to lower levels of pro-oxidative activity, higher levels of antioxidant activity and higher concentration of nitrite and nitrate. This combination may be responsible for the lower levels of BP in subjects with better physical fitness.

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35

Jones, Melanie. "Mechanisms Associated with Aging and Age-Related Disease in Drosophila". VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2110.

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Aging is an intrinsic process that is independent of obvious disease. In contrast to normal aging, age-related diseases are conditions that typically manifest at advanced ages, are associated with explicit pathology and cause disability and premature death. We used Drosophila as a model to investigate the molecular-genetic mechanisms associated with aging and age-related disease. Age-related locomotor impairment (ARLI) is a serious condition for the elderly and greatly impacts their quality of life. Toward identifying genes and mechanisms that influence ARLI, we performed a forward genetic screen using Drosophila mutants. This screen identified a loss of function mutant in PDK1, a component of the insulin signaling pathway. Additional loss of function mutants in the insulin signaling pathway genes PI3K Dp110, and AKT also delayed ARLI. These results suggest a role for insulin signaling in ARLI. Wolfram Syndrome (WFS) is a progressive neurodegenerative disease that is caused by mutations in the genes WFS1 and CISD2. The function of CISD2, the most recently identified gene has not been fully resolved. We used RNAi to knockdown wfs2, the fly ortholog of CISD2 to identify genes and pathways associated with wfs2 that will provide insight into the normal function of this gene. Through a targeted genetic screen in the Drosophila eye we identified that wfs2 interacts with two lysosomal storage disease genes PPT1 and CLN3. These results suggest that WFS and lysosomal storage diseases may be influenced by common molecular-genetic mechanisms. Furthermore, wfs2 may play a role in the neurodegenerative pathways associated with lysosomal storage disease. Oxidative stress is associated with aging and age-related disease. To identify genes that can protect against endogenous oxidative stress we performed a candidate suppressor screen. This screen revealed that expression of wild-type Ataxin-3 suppressed the short lifespan of Sod2 knockdown flies. The ubiquitin associated function of Ataxin-3 was determined to be important for this suppression. Interestingly, Ataxin-3 expression also extended the short lifespan due to knockdown of thioredoxin reductase in muscle. These results suggest that Ataxin-3 expression may play a protective role against enhanced endogenous oxidative stress due to reduced function of a number of antioxidant enzymes.

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Heemann, Fernanda Maciel. "Avaliação do estresse oxidativo em cérebro de ratas reprodutoras ao longo do envelhecimento". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/141964.

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A reprodução é uma fase crítica e exigente na vida dos animais. Nos mamíferos, as fêmeas costumam investir muito mais no cuidado parental do que os machos e a lactação é o período mais exigente em termos energéticos da vida da fêmea. Aqui, testamos se o estresse oxidativo é uma consequência da reprodução em ratas Wistar. Foram avaliadas as atividades da glutationa peroxidase, glutationa S-transferase, superóxido dismutase, o consumo de peróxido de hidrogênio, carbonilação de proteínas, peroxidação lipídica, níveis de nitrito e nitrato, glutationa total, níveis de vitamina C, bem como os níveis de estradiol no tecido cerebral em 3 , 6, 12, e 24 meses de idade. Os animais foram agrupados de acordo com a experiência reprodutiva: reprodutores ou não reprodutores. A maioria dos parâmetros estudados mostrou uma diferença entre animais não reprodutores e reprodutores de 12 e 24 meses. Aos 24 meses de idade animais reprodutores apresentaram maior atividade de superóxido dismutase, consumo de peróxido de hidrogênio, glutationa peroxidase e carbonilação de proteínas do que os animais não reprodutores. Aos 6 meses de idade, durante o período que representaria o pico da atividade reprodutiva, animais não reprodutores apresentaram níveis mais altos de malondealdeído. Em animais não reprodutores aos 12 meses de idade observou-se níveis mais altos de estrogênio, vitamina C, consumo de peróxido de hidrogênio e atividades de superóxido dismutase e glutationa peroxidase em relação aos animais reprodutores. Demonstramos que o processo de envelhecimento induz a uma elevação no dano oxidativo e também nas defesas antioxidantes em cérebro de ratas reprodutoras, sendo de alguma forma, a reprodução um processo custoso. Este estudo mostra que existe um forte potencial para a investigação do custo reprodutivo e estresse oxidativo.
Reproduction is a critical and demanding phase of the animals’ life. In mammals, females usually invest much more in parental care than males and lactation is the most energetically demanding period of a female’s life. In this work, we tested whether oxidative stress is a consequence of reproduction in female Wistar rats. We evaluated the activities of glutathione peroxidase, glutathione S-transferase, superoxide dismutase, consumption of hydrogen peroxide, protein carbonylation, lipid peroxidation, nitrite and nitrate levels, total glutathione, vitamin C levels, as well as sex hormone levels in brain tissue at 3, 6, 12, and 24 months of age. Animals were grouped according to reproductive experience: breeders or non-breeders. The parameters studied showed a difference between non-breeders and breeders animals at 12 and 24 months. At 24 months of age breeders animals showed higher superoxide dismutase activity, consumption of hydrogen peroxide, glutathione peroxidase and carbonyl level than non-breeders animals. At 6 months of age, during the period that represents peak reproductive activity, non-breeders animals showed higher levels of malondialdehyde. In non-breeders animals at 12 months of age we observed a higher level of estrogen, vitamin C, consumption of hydrogen peroxide, superoxide dismutase and glutathione peroxidase activities than breeders animals. Finally, we demonstrated that the aging process causes higher oxidative damage and higher antioxidant defenses in brain of breeders female rats, being the reproduction process costly somehow. This study shows that there is strong potential for research linking the cost of reproduction and oxidative stress.

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37

Poppe, Sandra Castro. "Estresse oxidativo e envelhecimento". Universidade de São Paulo, 2001. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-11032019-102753/.

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Este trabalho enfatiza o estabelecimento de parâmetros relacionados ao estado de estresse oxidativo em uma população de idosos, avaliando-se: níveis de antioxidantes de baixo peso molecular no plasma, vitC, αTC e βCT assim como a sua ingestão alimentar diária; atividade das enzimas antioxidantes eritrocitárias (CuZn-SOD, CAT e GPX) níveis de produtos derivados da oxidação de lipídios, mais especificamente as substâncias reativas ao ácido tiobarbitúrico (SRAT) e a atividade do burst oxidativo em neutrófilos sanguíneos. Foram estudados 90 idosos, residentes na comunidade, com idade igual ou superior a 65 anos, selecionados a partir de uma sub-amostra do projeto EPIDOSO sob acompanhamento regular no Centro de Estudos do Envelhecimento da Universidade Federal de São Paulo. Os parâmetros acima foram comparados aos de uma população adulta jovem saudável (40-49 anos). A ingestão alimentar diária de vitC, vitE e βCT, na população idosa é bastante superior em relação ao grupo de adultos jovens e, também, superior às RDA (recomendações dietéticas diárias). Isto, provavelmente, se deve à orientação clínica e nutricional a que esta população idosa vem sendo submetida, ao longo do tempo. Este dado reforça a importância de um acompanhamento clínico sistemático e diferenciado para o indivíduo idoso. Apesar da adequada ingestão diária de antioxidantes, pela dieta, as concentrações plasmáticas encontradas não se correlacionam com a ingestão, e são inferiores, às concentrações plasmáticas encontradas na população de adultos jovens. Estes resultados indicam que, uma dieta ainda que equilibrada e adequada, não proporciona, concentrações plasmáticas de antioxidantes em idosos, adequadas para controlar a atividade de espécies oxidantes. Estas baixas concentrações plasmáticas de vitC, αTC e βCT, encontradas nos idosos, podem ser atribuídas à diferenças na absorção, distribuição e biodisponibilidade destes antioxidantes, próprias do envelhecimento. A atividade específica das enzimas antioxidantes são superiores às da população de jovens. Além disso, os parâmetros oxidativos são maiores na população idosa, reforçando a idéia do estresse oxidativo presente no envelhecimento. Esses idosos (90) foram submetidos a uma suplementação vitamínico-mineral diária de 800mg de αTC, 15mg de βCT, 2g de vitC e 100 µg de selênio, para observarmos modificações nos parâmetros oxidantes. O estudo de suplementação, randomizado, duplo-cego e controlado por placebo, foi desenhado da seguinte forma: os idosos foram divididos em 2 grupos de tratamento, T1 e T2, onde T1 recebeu inicialmente a suplementação vitamínico-mineral (100 dias) e, depois do período de washout (período em que os parâmetros medidos retornam para os valores basais) recebeu suplementação com placebo (100 dias). O tratamento T2 apresentou desenho inverso (cross-over) ou seja, recebeu a suplementação placebo nos primeiros 90 dias e nos últimos 90 dias recebeu a suplementação vitamínico-mineral. A análise dos resultados após a suplementação vitamínico-mineral demonstra, para T1 e para T2, um aumento nas concentrações plasmáticas de antioxidantes acompanhado de uma diminuição na atividade das enzimas antioxidantes implicando, possivelmente, uma resposta adaptativa da célula. Os parâmetros oxidativos determinados (SRAT e burst oxidativo de neutrófilos) diminuíram com a suplementação.
This work emphasizes the setting of oxidative stress-related parameters in a population of aged individuals, evaluating: plasmatic levels of low molecular weight antioxidants, vitamin C, α-tocopherol (αTC) and β-carotene (βCT) as well as their daily intake; activity of erythrocyte antioxidant enzymes (CuZnSOD, CAT and GPX); lipid oxidation-derived products, more specifically thiobarbituric acid-reactant substances, and blood neutrophil oxidative burst activity. We studied 90 aged subjects living in the community, with ages 65 or more, selected from a subsample of EPIDOSO project under regular supervision by the Centro de Estudos do Envelhecimento of Universidade Federal de São Paulo. The parameters above mentioned were compared to those of a healthy young adult population. The daily intake of vitC, vitE and βCT of the aged population is well above that of young adults, and also above the RDA This is probably due to the clinical and nutritional orientation that has been offered to this aged group. This fact attests to the importance of systematic and specific clinical counseling to the elderly. Despite the proper daily intake of antioxidants, the plasmatic concentrations of these antioxidants do not correlate to their intake, being lower than the plasmatic concentrations in young adults. These results suggest that even a balanced and adequate diet is not enough, in the elderly, to promote the plasmatic antioxidant concentration needed to contral the activity of oxidant species. These low plasma levels of vitC, vitE and βCT in the elderly can be attributed to changes in absorption, distribution, and bioavailability of these antioxidants, which are common in the aging process. The specific activities of the antioxidant enzymes are higher than those of the younger population. Additionally, the oxidative parameters are higher in the aged group, supporting the idea that oxidative stress is involved in the aging process. These aged subjects received a vitamin-mineral supplementation (800 mg αTC, 15 mg βCT, 2g vitC and 100 µg selenium) aiming to modify the oxidative parameters. The randomized, double blind and placebo-controlled supplementation study was thus designed: the aged subjects were divided in 2 treatment groups, T1 and T2, where T1 received, first the vitamin-mineral supplementation (100 days) and then, after a washout period, a placebo treatment (100 days). The T2 group received the same treatment, but in inverse order (cross-over). The result analysis shows an increase in the plasmatic antioxidant concentrations in both treated groups, as well as a decrease in the activities of the antioxidant enzymes, hinting to an adaptive cellular response. The supplementation also decreased the assessed oxidative parameters (SRAT and neutrophil oxidative burst).

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38

Cuevas, González Santiago. "Análisis de los factores de riesgo cardiovascular en el proceso de envejecimiento y su relación con el estrés oxidativo. Estudio piloto observacional". Doctoral thesis, Universidad de Murcia, 2008. http://hdl.handle.net/10803/10861.

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Estrés oxidativo e inflamación parecen jugar un papel importante en el proceso de envejecimiento relacionado con la disfunción del sistema cardiovascular humano. Hábitos de vida tales como fumar, consumo de alcohol y ejercicio físico, pueden alterar el estado redox de los tejidos y afectar la relación de los marcadores de estrés oxidativo con la edad. Se requiere Información sobre el estado oxidativo de las poblaciones humanas para verificar la función de daño oxidativo en el envejecimiento y los cambios relacionados con el sistema cardiovascular, con el fin de identificar cuáles son los factores de riesgo cardiovascular más influyentes en el daño oxidativo asociado al envejecimiento y el papel de la dieta y el estilo de vida en esta relación. Este estudio se realizó en una población de 160 personas sanas o con patología leve tratada y compensada, distribuidos uniformemente en un rango de edad de 16 a 84 años. Lo datos recogidos de cada paciente fueron; antropométricos, bioquímica general, personales, dietéticos y se determinó la concentración de variables relacionadas con el estrés oxidativo, inflamación y/o riesgo cardiovascular: Mieloperoxidasa (MPO), Homocisteina, Proteína C Reactiva (PCR) ultrasensible y Malondialdehido (MDA). Resultados. La edad se correlaciona con numerosos marcadores de riesgo cardiovascular aunque no lo hace con los de estrés oxidativo. La PCR, la MPO y el MDA se correlacionan positivamente con los triglicéridos. El MDA se correlaciona con el colesterol; la PCR con el Índice Aterogénico; el IMC y la circunferencia de cintura resultaron las variables que más influyen sobre la concentración de triglicéridos e Índice aterogénico. El MDA se correlaciona positivamente con la edad en individuos menores de 65 años. El consumo de frutas y verduras se asociaría negativamente al MDA en una regresión múltiple incluyendo solo individuos de 40 a 65 años. Los resultados de este estudio indican que las variables lipídicas son las que mejor se correlacionan con el estrés oxidativo. El IMC y la circunferencia de cintura se han comportado como las variables más influyentes sobre los valores de lipídicos. Los hábitos dietéticos relacionados con el consumo de frutas y verduras ayudan a disminuir la concentración de MDA que tiende a incrementarse con la edad en individuos de 40 a 65 años en nuestra población.
Oxidative stress and inflammation appear to play an important role in the process of ageing and in the associated dysfunction of the human cardiovascular system. Lifestyle habits such as smoking, alcohol consummation, physical exercises, might alter the redox state of body tissues and affect the relationship of oxidative stress markers with age. Information about the oxidative status of human populations is required to verify the role of oxidative damage in the ageing related changes of the cardiovascular system, and to identify what are the most influential cardiovascular risk factors on the oxidative damage associated to ageing and the influence of lifestyle in this relation. This study was conducted in a population of 160 healthy individuals or with mild disease treated and compensated, in an evenly distributed range of age of age 16 to 84 years. General biochemical, anthropometric data, personal, dietary supplements and determining the concentration of variables related to oxidative stress and / or cardiovascular risk: Myeloperoxidase (MPO), Homocysteine, ultrasensitive C-reactive protein (CRP) and Malondialdehyde (MDA) was collected of each patient. Information about individual lifestyle patterns were also collected. Interactions between variables were assessed by correlation (Pearson or Spearman) and multiple regression analyses. Results. There were not gender differences in the variables of oxidative stress and inflammation assessed in this study. hsCRP was significantly associated with age, Framingham index, waist circumference, body mass index, blood glucose and plasma triglycerides. MDA plasma concentration was related to the values of cholesterol and triglycerides blood levels. MPO was associated with the plasma concentration of triglycerides and the atherogenic index. BMI and waist circumference are variables with more influence in the concentration of triglycerides and atherogenic index. The MDA was positively correlated with age in individuals younger than 65 years. The consumption of fruits and vegetables were negatively associated with MDA in a multiple regression including only individuals from 40 to 65 years. These results indicate that plasma concentrations of triglycerides and total cholesterol positively associate with oxidative stress and inflammation in a general human population. In addition, due to the body mass index appears to be the most influential factor on the lipid plasma levels, it may be a good marker of this association. Eating habits associated with the consumption of fruits and vegetables help reduce the concentration of MDA, which tends to increase with age in individuals 40 to 65 years in our population.

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39

Stab, II Bernd Robert. "The Effects of Cell Culture Oxygen Levels on the Replicative Senescence Processes of Primary Human Fibroblasts". Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/28468.

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Serial passaging of primary human fibroblasts leads to the formation of non-dividing senescent cells by a process termed replicative senescence. This tissue culture-based methodology is currently used as a model system to determine the underlying mechanisms of in vivo cellular aging and tumor suppression. Senescence is regarded as an alternative pathway to apoptosis, where cells undergo multiple changes in metabolic and cellular signaling pathways in order to prevent proliferation but still maintain a metabolically-active cell. Whether or not this model accurately reflects in vivo processes is presently controversial; however, replicative senescence is currently the most applicable model through which one can investigate the underlying causes of human cellular aging in the context of controlled environmental stress over time. This work was directed at understanding the molecular processes involved in replicative senescence with specific emphasis on the role of the mitochondria. A series of experiments were performed to assess changes during the induction of replicative senescence under conditions of low (3%) and high (20%) oxygen levels. Measurements were made at the transcriptional, protein, and metabolite levels. Microscopy wasalso utilized to monitor changes in mitochondrial morphology and volume. While previous studies have evaluated specific pathways and/or products; this work combines a more complete metabolomic, genomic, proteomic, and morphological picture of cells undergoing senescence and oxidative stress. Considering the low cell population densities of primary adherent fibroblasts and the subsequent low concentrations of small polar metabolites involved in glycolysis and the TCA cycle, methodologies needed to be developed in order to optimize metabolite extraction and liquid chromatography-mass spectrometric analysis. Protein kinase and transcriptional microarrays were also performed in order to quantify the changes in activated/deactivated signaling cascades as well as gene expression and relate these findings to metabolomic data. Mitochondrial dynamics of cells at different age time points and under different oxygen conditions were also assessed including mitochondrial size, shape, membrane potential, and percent volume per cell volume using confocal microscopy. The results obtained not only confirm the major pathways involved in senescence (p53/p21, PTEN/p27, and RTK/Raf/MAPK) but also provide evidence at both the transcriptional and protein levels for additional senescence-associated pathways. The majority of the changes observed were related to pathways involved in cellular stress, cell cycle control, and the survival response. Metabolic data suggested a –pooling effect– of glycolysis and TCA precursor molecules due to attenuation in enzyme function; this theory was also supported by an observed up regulation of gene expression as a compensatory mechanism. Mitochondria exhibited changes in membrane potential as well as volume and percent volume per cell which suggested compensatory hypertrophy and/or attenuation of mitochondrial fission processes. When the aforementioned analyses are tied together, a “theoretical model of senescence” can be formulated and is characterized by increased metabolic protein and associated metabolite levels due to attenuation in their respective enzyme function, resulting in increases in expression of their associated genes as a compensatory mechanism.
Ph. D.

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40

Opii, Wycliffe Omondi. "Oxidative stress and redox proteomics studies in models of neurodegenerative disorders I. the canine model of human aging ; II. insights into succesful [sic] aging ; and III. traumatic brain injury /". Lexington, Ky. : [University of Kentucky Libraries], 2006. http://lib.uky.edu/ETD/ukychem2006d00520/Final.pdf.

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Thesis (Ph. D.)--University of Kentucky, 2006.
Title from document title page (viewed Jan. 29, 2007). Document formatted into pages; contains: xviii, 430 p. : ill. (some col.). Includes abstract and vita. Includes bibliographical references (p. 353-426).

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41

Medlow, Paul Wallace. "The effects of aerobic exercise on oxidative stress and cardiovascular risk factors in aging and type II diabetes mellitus". Thesis, University of Ulster, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.601214.

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The oxidation of low-density lipoproteins (LDL) is considered a key step in the development and progression of atherosclerosis. Single bouts of aerobic exercise cause transient increases in free radical production that may enhance the susceptibility of LDL to oxidation and create a more atherogenic LDL particle. In contrast, chronic exercise has often been considered an effective tool in improving metabolic profile through changes in aerobic capacity, lipid profile, fuel utilization and oxidative stress in both healthy and disease populations. Despite this, less is known about how it may benefit the prevention of LDL oxidation and the mechanisms by which this may occur, particularly in aged and patients with type II diabetes who have oxidative stress. The primary aim of the work contained in this thesis, is to examine the effects of aerobic exercise on the susceptibility of LDL to oxidation in both young, aged and type II diabetic subjects. The findings of study 1 demonstrate that an acute bout of moderate intensity exercise can increase the susceptibility of LDL III in both young and aged subjects regardless of any change in LDL lipid composition. Study 2 demonstrates that chronic aerobic exercise of moderate intensity is effective at improving the resistance of the LDL I sub fraction against oxidation, as shown by an increase in T1I2max, despite no change in LDL lipid composition. This intervention was also beneficial in altering maximal aerobic capacity in both young and aged subjects. Study 3 demonstrates that chronic low and moderate intensity aerobic exercise has no effect on LDL oxidative susceptibility. However, chronic moderate intensity exercise increased catalase activity and decreased protein oxidation. The collective findings of this work provide evidence that acute exercise may increase LDL oxidation while chronic exercise may prevent the oxidation of LDL particularly in aged subjects. Further research with greater subject numbers is required to determine the precise mechanism by which exercise influences the susceptibility of LDL oxidation.

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42

Hindle, Allyson Gayle. "An evaluation of the impacts of aging on skeletal muscle performance in several mammalian divers". [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-2615.

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43

Fu, Yu. "Modulating effects of Chinese green tea on hippocampal neurons against glutamate neurotoxicity and hippocampal dependent memory during aging in mice". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B32017893.

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44

Martin, Ian. "Effects of Altered Superoxide Dismutase Expression on Age-related Functional Declines and Survival in Drosophila". VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1589.

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Most organisms experience progressive declines in physiological function as they age. A number of studies in a variety of species support a strong link between oxidative damage, age-related functional declines and life span determination. Here, manipulating the expression levels of superoxide dismutase (SOD) isoenzymes SOD1 and SOD2, resulted in altered functional senescence and survival characteristics in Drosophila. Overexpression of cytosolic Sod1 using the yeast GAL4/UAS system conferred a 30-34% increase in mean life span and resulted in an attenuated senescence of odor avoidance behavior in aging flies. Tissue-specific Sod1 overexpression selectively in the nervous system or muscle failed to reproduce these delayed aging phenotypes suggesting that Sod1 overexpression in these tissues alone was not primarily responsible for the aging effects observed. Graded reduction of mitochondrially localized Sod2 expression in a series of Sod2 mutants led to progressive reductions in life span, accelerated age-related functional declines, mitochondrial oxidative damage and neuronal cell death. Tissue-specific Sod2 knock-down using RNA interference revealed that muscle is a key tissue underlying the accelerated age-related functional decline and mortality observed upon loss of SOD2. Sod2 knock-down in the musculature caused a degenerative phenotype consisting of a dramatic reduction in muscle mitochondrial content and ATP levels, elevated cell death and progressive locomotor dysfunction which culminated in early-onset mortality. Collectively, these studies highlight the important role of SOD enzymes in protecting against the impact of oxidative damage on senescence and survival. These findings also lend further support to the oxidative damage hypothesis of aging.

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45

Corenblum, Mandi J., Sneha Ray, Quentin W. Remley, Min Long, Bryan Harder, Donna D. Zhang, Carol A. Barnes y Lalitha Madhavan. "Reduced Nrf2 expression mediates the decline in neural stem cell function during a critical middle-age period". WILEY-BLACKWELL, 2016. http://hdl.handle.net/10150/622598.

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Although it is known that the regenerative function of neural stem/progenitor cells (NSPCs) declines with age, causal mechanisms underlying this phenomenon are not understood. Here, we systematically analyze subventricular zone (SVZ) NSPCs, in various groups of rats across the aging spectrum, using in vitro and in vivo histological and behavioral techniques. These studies indicate that although NSPC function continuously declines with advancing age, there is a critical time period during middle age (13-15 months) when a striking reduction in NSPC survival and regeneration (proliferation and neuronal differentiation) occurs. The studies also indicate that this specific temporal pattern of NSPC deterioration is functionally relevant at a behavioral level and correlates with the decreasing expression of the redox-sensitive transcription factor, Nrf2, in the NSPCs. When Nrf2 expression was suppressed in 'young' NSPCs, using short interfering RNAs, the survival and regeneration of the NSPCs was significantly compromised and mirrored 'old' NSPCs. Conversely, Nrf2 overexpression in 'old' NSPCs rendered them similar to 'young' NSPCs, and they showed increased survival and regeneration. Furthermore, examination of newborn Nrf2 knockout (Nrf2-/-) mice revealed a lower number of SVZ NSPCs in these animals, when compared to wild-type controls. In addition, the proliferative and neurogenic potential of the NSPCs was also compromised in the Nrf2-/- mice. These results identify a novel regulatory role for Nrf2 in NSPC function during aging and have important implications for developing NSPC-based strategies to support healthy aging and to treat age-related neurodegenerative disorders.

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46

Wood, Emma Mary. "Causes and fitness consequences of telomere dynamics in a wild social bird". Thesis, University of Exeter, 2017. http://hdl.handle.net/10871/29777.

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Telomeres are increasingly used as biomarkers of somatic maintenance and could conceivably play a causal role in life history trade-offs. In this thesis, I use longitudinal telomere measures from a wild population of cooperatively breeding white-browed sparrow weavers (Plocepasser mahali) to further our understanding of the causes and fitness consequences of individual variation in somatic maintenance, with particular focus on hitherto unexplored effects of the social environment. In Chapter 2, I start by investigating the key prediction of life-history theory that shortfalls in somatic maintenance in early life entail later-life costs, and find supporting evidence. Nestlings with higher within-individual rates of telomere attrition show reduced survival to the following season, even after controlling for the effects of variation in body mass. In Chapter 3, I then investigate the effects of the social and abiotic environment on nestling telomere length and attrition rates and find the first support, to my knowledge, for the key prediction that helpers in cooperatively breeding societies alleviate telomere attrition rates in growing offspring (consistent with the expectation that helper contributions to nestling feeding relax resource allocation trade-offs in offspring). In addition, I find that rainfall prior to egg-laying has a positive effect on hatchling telomere length; an effect that most likely arises via egg- or incubation-mediated maternal effects. In Chapter 4, I investigate the causes of variation in telomere attrition rates in adults, and while there are no overall differences in telomere length or long-term within-individual telomere dynamics between dominant and subordinate birds, my findings are suggestive of dominance-related differences in the short-term regulation of telomere length. In addition, and in concordance with predictions of life-history theory regarding trade-offs between somatic maintenance and reproduction, I find that annual rainfall (a proxy for reproduction-related activity during the breeding season) negatively predicts the within-individual rate of change in telomere length in adults specifically over the breeding season; there was no such relationship in the non-breeding season. Finally, in Chapter 5, I investigate the extent to which natural variation in oxidative state predicts variation in within-individual rates of change in telomere length over time. This chapter provides evidence suggestive of associations between oxidative state and telomere dynamics in a natural population, and highlights complexity in the nature of these relationships. Together my findings provide novel support for key predictions of life-history theory regarding the causes and consequences of variation in somatic maintenance, and lend strength to the view that longitudinal field studies of telomere dynamics can offer useful insights in this regard. Furthermore, my findings highlight the potential for diverse effects of the social environment on patterns of somatic maintenance, and specifically hitherto unexplored downstream effects of helping behaviour on later-life performance and ageing trajectories.

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47

Ha-Ahn, Tung. "Influence du vieillissement thermo-oxydatif sur les comportements mécaniques du polychloroprène Influence of thermo-oxidative aging on the mechanical behaviors of polychloroprene /". [S.l. : s.n.], 2007.

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48

Silva, Ana Carolina Almeida da. "Estresse oxidativo em rins de ratas reprodutoras e não reprodutoras ao longo do envelhecimento". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/78149.

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A reprodução é um processo dispendioso da vida, e o investimento reprodutivo parece ser maior para fêmeas do que para os machos em muitas espécies. Neste trabalho analisamos os efeitos do investimento reprodutivo durante o envelhecimento com relação aos parâmetros de estresse oxidativo em rins de ratas Wistar. Medimos a atividade da glutationa peroxidase, glutationa S-transferase, superóxido dismutase e aconitase. O consumo de peróxido de hidrogénio, a carbonilação de proteínas, peroxidação lipídica, nitrito e nitrato, os níveis de vitamina C e E e de hormônios sexuais foram também mensurados. Traçamos o perfil oxidativo nas idades de 3, 6, 12 e 24 meses. Os animais foram agrupados de acordo com a experiência reprodutiva: em reprodutores e não reprodutores. Os animais não reprodutores exibiram um aumento nos parâmetros estudados aos 6 e 24 meses, enquanto que os animais reprodutores exibiram um perfil semelhante aos 3 e 12 meses. Aos seis meses de idade, durante o período que representa o pico reprodutivo, os animais não reprodutores apresentaram maiores níveis de MDA, vitamina C, consumo de peróxido de hidrogênio e atividades de GPx, aconitase e SOD. Em ratos idosos não reprodutores, observou-se um aumento nos marcadores de dano oxidativo e um aumento nas defesas antioxidantes enzimáticas e não enzimáticas, com a exceção do consumo de peróxido de hidrogênio e vitamina C. Em longo prazo, pode-se inferir que o investimento reprodutivo não foi suficiente para interferir com a capacidade antioxidante, e não contribuiu para o dano oxidativo em rins de ratas Wistar.
Reproduction is a costly life process, and the reproductive investment by females appears to be greater than males in many species. We have analyzed the effects of reproductive investment during aging with respect to oxidative stress parameters in kidneys of female Wistar rats. We measured the activity glutathione peroxidase, glutathione S-transferase, superoxide dismutase, consumption of hydrogen peroxide, protein carbonylation, lipid peroxidation, nitrite and nitrate levels, and vitamin C and E levels. We traced oxidative profiles at ages 3, 6, 12, and 24 months. Animals were grouped according to reproductive experience: experienced or naïve with respect to reproductive activity. We measured aconitase activity and sex hormone levels. The naïve animals exhibited an increase in the parameters studied at 6 and 24 months, whereas experienced animals exhibited a similar increase at 3 and 12 months. At six months of age, during the period that would represent peak reproductive activity, naïve animals showed higher levels of MDA, Vitamin C, consumption of hydrogen peroxide and GPx, aconitase, and SOD activities. In naïve elderly rats, we observed an increase in oxidative damage markers and an increase in enzymatic and non-enzymatic antioxidants, with the exception of consumption of hydrogen peroxide and vitamin C. In the long term, the reproductive investment was not sufficient to interfere with antioxidant capacity, and did not contribute to oxidative damage in kidneys of female Wistar rats.

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49

Paniz, Clóvis. "Avaliação do estado micronutricional e de estresse oxidativo em idosos". Universidade Federal de Santa Maria, 2007. http://repositorio.ufsm.br/handle/1/11154.

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The increase in life expectancy has made the aging of the population a global phenomenon. Projections point to a growth of greater than 300% in the number of elderly people over the next 50 years. The rapid growth of the elderly population, mainly in developing countries has become a public health problem. In this age group, non transmissible chronic diseases are very common, mainly those of a nutritional origin. Although aging is a complex phenomenon, oxidative stress seems to play an important role in this process. On the other hand, there are few studies evaluating the levels of antioxidants in the diet and oxidative stress biomarkers in healthy elderly. These data could be useful to understand the role of oxidative stress in physiopathological changes associated with human aging, both in institutionalized elderly and in non-institutionalized elderly. In the this study, an analysis was made of oxidative stress biomarkers such as reduced glutathione (GSH), malondialdehyde (MDA), protein carbonyls (PCO) and δ-aminolevulinate dehydratase (ALA-D) as well as, some antioxidants from the diet such as vitamin C, E, B12 and folate; of in institutionalized elderly women (n= 45; 71 ± 6 years old) from a public retirement home and non-institutionalized elderly women (n= 22; 68 ± 6 years old). Moreover, the nutritional status was evaluated through a determination of serum albumin, hemoglobin and the body mass index (BMI) as well as a lipidic profile. The mental state was assessed through the Mini Mental State Examination (MEEM). In the institutionalized group, vitamin C levels were significantly decreased and vitamin E levels were significantly increased. The levels of folate and vitamin B12 did not show significant differences between the groups and a low deficiency incidence was found for both vitamins. However, both vitamins were within the normal range established for adults. GSH and PCO did not present significant differences between the groups, while MDA and ALA-D were significantly increased in the non-institutionalized group. The institutionalized group had a lower cognitive performance, showing scores significantly decreased. Moreover, positive correlations were found between vitamin C and ALA-D, vitamin C and albumin, vitamin C and hemoglobin, vitamin C and the mental state and between folate and MEEM. Moreover, a negative correlation was found between vitamin E and both PCO and MDA, between PCO and ALA-D and between ALA-D and age. Thus, through the results found in the institutionalized elderly women, it can be suggested that the evaluated micronutrient levels, considered normal for adults, could be insufficient for the elderly. Vitamin C may protect some blood proteins from oxidative effects, especially those with thiol groups. Vitamin E levels may have an effect on MDA levels, protecting the lipid membrane from lipoperoxidation, and also, the carbonylation of proteins. In addition, both vitamin C and folate demonstrated protection against cognitive impairment in elderly women. The ALA-D was presented as a possible oxidative stress biomarker to evaluate oxidative stress in elderly.
O aumento da expectativa de vida tornou o envelhecimento populacional um fenômeno global. O rápido crescimento da população idosa, principalmente em países em desenvolvimento, tem se tornado um problema de saúde pública. Apesar de o envelheci-mento ser um fenômeno complexo, o estresse oxidativo parece desempenhar um papel importante sobre este processo. Por outro lado, existem poucos estudos avaliando os níveis de antioxidantes da dieta, bem como, os marcadores do estresse oxidativo em idosos saudáveis. Estas informações podem ser úteis para entender o envolvimento do estresse oxidativo nas mudanças fisiopatológicas associadas ao envelhecimento humano, tanto em idosos institucionalizados como em idosos não institucionalizados. Neste estudo foram analisados marcadores do estresse oxidativo, como glutationa reduzida (GSH), malondialdeído (MDA), proteínas carboniladas (PCO), δ-aminolevulinato desidratase (ALA-D) e alguns micronutrientes da dieta como vitaminas C, E, B12 e folatos no sangue de idosas institucionalizadas (n= 45; 71 ± 6 anos), em asilos públicos de Santa Maria, e idosas não institucionalizadas (n=22; 68 ± 6 anos), pertencentes a grupos de terceira idade. Além disso, foi avaliado o estado nutricional, através das determinações de albumina, hemoglobina e do índice de massa corporal (IMC); o perfil lipídico; e o estado mental, verificado através do Mini-Exame do Estado Mental (MEEM). Os níveis de vitamina C foram significativamente menores nas institucionalizadas, enquanto os níveis de vitamina E foram significativamente maiores neste grupo. Os níveis de folatos e vitamina B12 não mostraram diferenças significativas entre os grupos e uma baixa incidência de deficiência de ambas foi encontrada. Todas as vitaminas determinadas estavam dentro dos valores estabelecidos como de referência para adultos. GSH e PCO, não mostraram diferenças significativas entre os grupos, enquanto MDA e ALA-D foram significativamente aumentadas nas idosas não institucionalizadas. As idosas institucionalizadas tiveram pior desempenho cognitivo avaliado pelo MEEM, mostrando escores significativamente menores. Além disso, foi encontrada uma correlação positiva entre vitamina C com ALA-D; com albumina; com hemoglobina; e com MEEM; e entre folatos e MEEM. Foi encontrada correlação negativa entre vitamina E com PCO e com MDA; PCO com ALA-D e ALA-D com idade. Através dos resultados obtidos, sugere-se que os níveis de micronutrientes encontrados em nosso estudo, embora considerados normais para adultos, poderiam ser insuficientes para idosos. A vitamina C parece proteger algumas proteínas sanguíneas com grupos tiólicos como ALA-D e albumina, enquanto a vitamina E parece proteger estruturas lipídicas do ataque oxidativo. Em adição, as vitaminas C e os folatos parecem proteger contra perdas cognitivas em idosas. A atividade da ALA-D sangüínea mostrou ser um marcador útil para avaliação de estresse oxidativo em idosos.

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50

Vaishnav, Radhika Anand. "MOLECULAR MECHANISMS OF OLFACTORY NEURODEGENERATION". UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_diss/669.

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Olfactory sensory decline has been associated with normal aging as well as neurodegenerative disorders, yet the underlying mechanisms are unclear. The overall aim of this dissertation was to investigate the fundamental molecular and cellular mechanisms associated with olfactory neurodegeneration. This investigation uses an integrative approach, combining proteomics and gene expression analyses with cellular and tissuelevel characterization. Using these approaches, two model systems were investigated: 1) normally aging C57BL/6 mice of ages 1.5-, 6- and 20-months; and 2) a mouse model of elevated endogenous oxidative stress-associated neurodegeneration, namely, the Harlequin mutant mouse. The first specific aim was to test the hypothesis that oxidative stress is associated with aging of the olfactory system. Using proteomics, I demonstrated that olfactory aging was accompanied primarily by increased oxidative stress-, mitochondrial metabolism- and synaptic/transport-associated changes. The second specific aim was to test the hypothesis that the olfactory system accumulates oxidative stress-mediated macromolecular damage over time, predisposing it to neurodegeneration. Two types of protein oxidation, namely, carbonylation and nitration, accumulated with aging in the olfactory system. Protein and cellular targets of oxidative stress-associated damage were identified using redox proteomics coupled with immunohistochemical localization. The third specific aim was to test the hypothesis that elevated oxidative stress in the olfactory system results in apoptosis/neurodegeneration. The Harlequin mutant mouse was critically selected and validated as a model for studies of oxidative stress-associated olfactory neurodegeneration at both the cellular and molecular levels. The Harlequin mouse had decreased levels and altered distribution of apoptosis inducing factor protein in mature olfactory sensory neurons, increased oxidative DNA damage and apoptosis in the olfactory epithelium, and pronounced cytoskeletal disorganization. The molecular studies confirmed and extended our cellular data and identified several significantly regulated genes associated with elevated oxidative stress and apoptosis. This novel study, by combining contemporary proteomics and genomics with cellular and tissue-level analyses, has provided a road map for understanding fundamental molecular mechanisms of olfactory degeneration.

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