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Chan, Wai-ho. "Study on the role of osmotic stress, oxidative stress and poly(ADP-ribose) polymerase in the pathogenesis of diabetic cataract." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36371725.
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Chan, Wai-ho, and 陳韋豪. "Study on the role of osmotic stress, oxidative stress and poly(ADP-ribose) polymerase in the pathogenesis of diabetic cataract." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36371725.
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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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Dewar, Mairead. "Oxidative stress and cardiovascular ageing in diabetes." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29910.
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Oxidative stress is thought to be elevated in diabetes as a consequence of hyperglycaemia. This thesis investigates oxidative DNA damage in diabetes, which may contribute to accelerated vascular ageing. Telomeric and mitochondrial DNA are two areas of the genome that may be more susceptible to oxidative stress and were therefore investigated.;51 patients with diabetes (aged 31-78 years) and 101 healthy controls (aged 19-75 years) were recruited. 51 of the controls were age- and sex-matched to be patient group. For both populations physiological profiles were obtained and pulse wave velocity (PWV), an index of vascular stiffness, was measured. Oxidative DNA damage was also investigated in peripheral blood using the comet assay, and in more depth by measuring terminal restriction fragment (TRF) lengths and quantifying mitochondrial DNA (mtDNA) content. PWV increased with age in both study groups (p<0.001) and was significantly higher in the patient group (8.00 +/- 2.89 versus 7.29 +/- 1.64 m/s; p=0.006), suggesting accelerated vascular ageing in diabetes. This was accompanied by elevated levels of oxidative DNA damage; 25.81 +/- 1.18 versus 21.40 +/- 0.81% Tail DNA (p=0.003) in patients and controls respectively. TRF length inversely correlated with age in both groups (p<0.05), with similar rates of attrition, and although they were shorter in the patients with diabetes, this was not significant (p=0.10). Quantification of mtDNA revealed significantly lower levels in the patients with diabetes compared to the controls (0.014 versus 0.016; p=0.020). There is accelerated vascular ageing in diabetes, which is accompanied by elevated oxidative DNA damage, and a decrease in mtDNA, but no alteration in TRF length compared to a healthy control population. The mechanisms underlying these alterations are unknown with the lack of correlations with glycaemic control suggesting it is not the sole cause but it may still contribute.
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Lassen, Natalie. "Roles of aldehyde dehydrogenases (ALDHs) against oxidative stress /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.
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Thesis (Ph.D. in Toxicology) -- University of Colorado at Denver and Health Sciences Center, 2006.Typescript. Includes bibliographical references (leaves 119-138). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Stephens, Jeffrey Wayne. "Genetic determinants of oxidative stress in diabetes mellitus." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446841/.
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Increased oxidative stress has been implicated in the pathogenesis of atherosclerosis and coronary heart disease, and is a key feature of diabetes mellitus. Increased oxidative stress has numerous adverse effects on the vascular system, including the altered expression of cell adhesion molecules, induction of pro-inflammatory mediators and more specifically the oxidation of low density lipoprotein (LDL) to form oxidised LDL (Ox-LDL). As well as measuring the total degree of oxidative stress in plasma, specific measures may also be recorded, such as the degree of LDL-oxidation. This thesis focuses on the association between plasma markers of oxidative stress and LDL-oxidation with other biochemical intermediate risk factors and common gene variants, in subjects with diabetes mellitus. Analysis focused on three candidate genes: a cellular anti-oxidant, glutathione-s-transferase; a plasma lipoprotein, apolipoprotein E; and a mitochondrial protein, uncoupling protein-2 (UCP2). The effect of common variants in these genes was explored in relation to plasma markers of oxidative stress, along with gene-environment interaction in the pro-oxidant environment of cigarette smoking. Initially a cohort of approximately 1000 subjects with diabetes, were recruited from the diabetes clinic at University College London Hospitals. Routine biochemical and clinical data was gathered, as well as plasma and blood for DNA extraction. Further in vitro functional studies were performed in respect to the UCP2 gene, to further our understanding of the role of this gene in the generation of oxidative stress and in the pathogenesis of coronary heart disease.
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Han, Bing. "Mechanistic Consequences of Cardiac Oxidative Stress." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1203478009.
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Catherwood, Mark Alexander. "Glucose-induced oxidative stress in vascular smooth muscle cells." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268225.
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Pitre, Deepali. "Oxidative mechanisms in diabetes related urinary bladder dysfunction." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1060880772.
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Hammerman, Malin. "Oxidative Stress and Protein Acetylation in Adipocytes." Thesis, Linköpings universitet, Proteinkemi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-75785.
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Obesity is an increasing health problem which is causally associated with insulin resistance and type 2 diabetes. Oxidative stress, i.e. overproduction of reactive oxygen species, is associated with insulin resistance and obesity and may be a major risk factor in the onset and progression of diabetes. Bernlohr Lab at University of Minnesota have study oxidative stress in adipocytes by silencing the enzyme glutathione S-transferase A-4 (GSTA4), an enzyme detoxifying 4-hydroxynonenal formed during oxidative stress. Their results indicate that lysine acetylation, an important post-translational modification, may be involved during oxidative stress. In this study lysine acetylation has been investigated in condition of oxidative stress in 3T3-L1 adipocytes and subcutaneous adipose tissue from mice using SDS-PAGE gel electrophoresis and western blot. Lysine acetylation was analyzed in different compartments of the cell such as in cytoplasm, mitochondria as well as in whole cell extracts. Silencing of GSTA4 and stimulation by TNF-α in 3T3-L1 adipocytes resulted in an increase of lysine acetylation in cytoplasm. Furthermore, stimulation by IL-6 did not have any effect on lysine acetylation. Surprisingly, subcutaneous adipose tissue from mice fed on a high-fat diet showed a decrease of lysine acetylation in cytoplasm compare to mice fed on a chow diet. In conclusion, lysine acetylation seems to change during oxidative stress and may be an important factor during insulin resistance, type 2 diabetes and obesity. Therefore, studying lysine acetylation and enzymes modulating acetylation may potentially increase our understanding of insulin resistance, type 2 diabetes and obesity and could lead to new therapies.
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Lal, Mark. "Oxidative stress and calcium signalling : implications for diabetes and cardiac glycosides /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-583-2/.
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Pariagh, Sandra. "Glucose metabolism in hepatocytes exposed to free radical stress." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341783.
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Herson, Paco S. "Oxidative stress activates a novel non-selective cation channel in insulin-secreting cells." Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265376.
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Single channel recordings from CRI-G1 insulin-secreting cells were used to characterize a novel ion channel. The presence of both Ca2+ and β-NAD+ at the cytoplasmic aspect of the membrane are required for channel activity. This is the first ion channel described which requires internal β-NAD+ for activity (thus termed NSNAD). The channel was found to be permeable to all monovalent (Na+, K+ and Cs+) and divalent cations tested (Ca2+, Mg2+, Ba2+, and Mn2+). The slope conductance is relatively large (70 - 90pS) compared to other non-selective cation channels and also has extremely slow kinetics (open and closed times in the range of seconds). Whole-cell voltage clamp experiments illustrate that internal β-NAD+ activates a cation current consistent with activation of the NSNAD channel. Similar to the single NSNAD channel, the β-NAD+-activated current was sensitive to the internal concentrations of both Ca2+ and β-NAD+. The non-selective nature of this cation current was confirmed by replacement of the internal K+ with Cs+ which did not diminish the β-NAD+-activated current. Additionally, replacement of external cations with the impermeant NMDG abolished the β-NAD+-activated current. The diabetogenic agent alloxan was found to irreversibly depolarize CRI-GI cells by opening a non-selective cation channel with characteristics similar to the NSNAD channel. The channel activated by alloxan is characterized by a slope conductance of approximately 70 pS and very slow (seconds) kinetics. Channel activity is lost upon excision of the patch, but can be re-activated by the application of internal β-NAD+. The mechanism of alloxan-induced depolarization and channel activation appears to be through the production of reactive oxygen species (ROS). This data indicates that oxidative stress generated by both alloxan and H2O2 causes the activation of the NSNAD channel which results in irreversible collapse of the membrane potential and massive Ca+ influx leading to eventual cell death. This may represent a component of the destruction of pancreatic β-cells during type I diabetes and possibly other pathologies in which oxidative stress is implicated.
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McGeoch, Susan Christina. "Effect of oats on post-prandial glycaemia, inflammation and oxidative stress in type 2 diabetes." Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158362.
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Acute post-prandial hyperglycaemia may trigger acute increases in systemic inflammation and oxidative stress, potential risk factors for cardiovascular disease. We aimed to investigate the effect of both an oat-rich diet and standard dietary advice on glycaemic control, post-prandial glycaemia, inflammation and oxidative stress in volunteers with diet-managed type 2 diabetes. Method In a randomised cross-over design 30 volunteers with type 2 diabetes followed for two 8 week periods either an oat-rich diet or a control diet based on standard dietary advice. Volunteers attended at baseline, week 8 and 16. Measurements included basic clinical parameters, baseline blood tests followed by consumption of a standard test-meal with glucose, insulin and markers of inflammation and oxidative stress quantified during the post-prandial period. During each dietary period volunteers underwent a three day period of free-living continuous glucose monitoring (CGMS) during which time they kept a food diary. At the study end, the post-prandial response to an iso-energetic meal rich in oats was assessed. Results There were no diet-related differences in parameters of glycaemic control or post-prandial glycaemia based on CGMS data. Dietary intervention also had no effect on either the glycaemic or insulinaemic responses to the test-meal and there were no differences in the acute responses to the standard or oat-based test meals. Chronic intervention with the oat-based diet increased fasting adiponectin concentrations (P=0.06) and post-prandial ORAC concentrations (P<0.05) but had no effect on fasting CRP, ORAC, OxLDL or TBARS concentrations or the post-prandial response of CRP, adiponectin or TBARS to the standard test-meal. Following the oat-based test meal, adiponectin concentrations declined less (P<0.05) while CRP concentrations increased less (P<0.05) compared with the standard test-meal. Conclusion The oat-rich diet exerted anti-inflammatory and anti-oxidant effects in both the basal and post-prandial states independent of any effect on glycaemia. These findings may have implications for nutritional management of cardiovascular risk.
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Spada, Ana Paula Machado [UNESP]. "Avaliação do estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada." Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/99250.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Objetivo: avaliar o estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada. Métodos: O diabete foi induzido em ratas Wistar recém-nascidas (grupo diabete moderado) no dia do nascimento (dia 0) por streptozotocin (100 mg/kg, via subcutênea). As ratas do grupo nãodiabético (controle) receberam somente tampão citrato. Na vida adulta, as ratas (diabéticas e controle) foram submetidas ao acasalamento e o dia de diagnóstico positivo de prenhez foi considerado dia 0. A glicemia foi determinada nos dias 0, 7, 14 e 21 de prenhez. No 21º dia de prenhez, as ratas foram anestesiadas e dessangradas para determinação das atividades enzimáticas de superóxido dismutase (SOD), glutationa peroxidase (GSH-Px) e glutationa redutase (GSH-Rd) e das concentrações de grupos tiólicos (SH) e de espécies reativas ao ácido tiobarbitúrico (TBARS). Em seguida, as placentas foram retiradas e processadas para determinação das atividades de SOD e catalase e concentração de TBARS, gluationa reduzida e grupos tiólicos. Resultados: Ratas com diabete induzido no período neonatal (grupo diabético) apresentaram glicemia superior a 120mg/dl no dia 0 de prenhez e foi observada hiperglicemia no 14º dia de prenhez. A análise do estresse oxidativo em hemáceas lavadas mostrou que no grupo diabético houve aumento significativo na atividade da GSH-Px. No tecido placentário a atividade da catalase foi significativamente maior em ratas com diabete moderado. Conclusão: Frente às condições experimentais analisadas, o aumento dos biomarcadores do sistema antioxidante em ratas com diabete de intensidade moderada foram suficientes para conter o estresse oxidativo.
Objective: To evaluate the oxidative stress in blood sample and placental of female rats that received streptozotocin in the neonatal period. Methods: The diabetes was induced in female offspring (diabetic group) in the day of the birth (day 0) for streptozotocin (100 mg/kg, subcutaneous route). Female control rat (control group) received only citrate buffer. In the adult life, the female rats were submitted to the mating and the day the positive diagnosis, was considered day 0 of pregnancy. The glycemia was measured in the 0, 7, 14 and 21 of pregnancy. At day 21 of pregnancy, the female rats were anesthetized and died by decapitation for collection of the blood for determination of the enzymatic activity of the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and of the concentrations of thiols group and thiobarbituric acid reactive substances (TBARS). Afterwards, placental were removed and processed for determinations of the enzymatic activity of the SOD and catalase and of the concentrations of the TBARS, glutathione reduced (GSH) and thiols group (SH). Results: Diabetic rats presented blood glucose concentration greater than 120 mg/dL in the day 0 of pregnancy and hyperglycemia in 14 º day of pregnancy. The analysis of the oxidative stress in maternal blood sample showed increased in GSH-Px activity. In placental tissue catalase activity of diabetic group is found to be increase in homogenate tissue in diabetic group. Conclusion: The hyperglycemia in diabetic rats increased antioxidant system biomarkers, however, these alterations were enough to control oxidative stress.
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Meigh, Heather Clare. "Models of oxidative stress induced by disease or pollution in invertebrates and vertebrates." Thesis, University of Plymouth, 2000. http://hdl.handle.net/10026.1/2393.
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Glutathione and its related enzymes have a central role in the antioxidant mechanisms of both invertebrates and vertebrates. Evidence suggests that changes in antioxidant defence mechanisms are associated with the late complications of diabetes. In addition, invertebrates show changes in antioxidant mechanisms in response to contamination; these changes have the potential to be utilised in the environmental monitoring of pollution. The present study investigated the role of glutathione and its related enzymes with regard to complications of diabetes and toxicity exposure using the crab, Carcinus maenas. A preliminary investigation showed that glutathione peroxidase and glutathione reductase activities are unaltered in the peripheral blood mononuclear cells from diabetic patients with long term complications of the disease. However, crabs were shown to have significantly reduced glutathione-s-transferase and glutathione peroxidase activities in response to cadmium exposure. The biochemical responses of crabs to pollution exposure were investigated in further experiments. Crabs are exposed to a variety of influences within their natural environment that may affect their ability to tolerate oxidative stress. These stressors include climatic changes, age, sex, nutritional status, contamination, accumulation of toxins and adaptation to a polluted environment. Results showed that seasonality also affects the activities of glutathione related enzymes glutathione reductase and glutathione-s-transferase, as well as physiological parameters such as tissue protein composition. Seasonal changes of enzyme activities may be partly due to the altered nutritional status of the crab over the year. Nutritional status also reduced the total glutathione status and total antioxidant scavenging ability of crab haemolymph and gill tissues. The levels of these parameters were reinstated to normal when the starved crabs were exposed to a mixed affluent. The ability to control the production of antioxidant scavenging compounds during fasting may help to preserve the crabs energy reserves. The promptly reinstated glutathione and total antioxidant scavenging ability in response to contamination helps to prevent the oxidative damage caused by pollution exposure. Several tissues were removed from the crab and the amount that each contributed to the crabs overall antioxidant scavenging ability was calculated. Haemolymph and muscle tissues were found to contribute the most to the crabs overall antioxidant scavenging ability. This is due to the large proportion of the crab that these tissues occupy. The level of glutathione within the crabs haemolymph, gill and muscle tissues did not contribute significantly to their overall antioxidant scavenging ability in normal conditions. However, when the stress was induced in the crabs in response to mixed effluent exposure or fasting, total glutathione levels became significantly correlated with total antioxidant scavenging ability. The results suggest that under these circumstances glutathione levels are maintained by the activity of glutathione reductase. A field trial was performed in the highly industrialised area of the Tees Estuary to establish whether the biomarkers that had been successfully applied in laboratory experiments could be used within the field. The results were analysed using multi-dimensional scaling techniques. This allowed a suite of biomarkers to be analysed simultaneously. The biomarker responses measured at the different sites indicated a gradient of toxicity from the top of the estuary to its mouth. These results were consistent with water chemical analysis data. The study showed that more information could be gained from this type of analysis than by examining the biomarker results separately. The biomarkers measured and the method of data analysis have potential to be used in routine toxicity assessment.
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Zhong, Wenwen. "Protection against oxidative stress in human endothelial cells in an in vitro diabetes model." Thesis, University of Hull, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431079.
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Le, Brocq Michelle Louise. "Advanced glycation end product precursors in diabetes : a crucial link between oxidative stress and inflammation?" Thesis, University of the Highlands and Islands, 2010. https://pure.uhi.ac.uk/portal/en/studentthesis/advanced-glycation-end-product-precursors-in-diabetes(53be96a1-0fe3-4fc7-88c7-2bf2b4421d27).html.
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Advanced glycated end-products (AGEs) are a heterogenous group of compounds formed through the Maillard reaction. During AGE formation, reactive α-dicarbonyls are formed, such as glyoxal (GO) and methylglyoxal (MG). These α-dicarbonyls are present at elevated concentrations in diabetes, and are frequently implicated in the initiation and progression of diabetic complications. Previous research has linked α-dicarbonyls with formation of reactive oxygen species (ROS) and inflammation. However, much of the prior work has been conducted using concentrations of α-dicarbonyls that are substantially higher than can be generated in vivo, and the biochemistry has been investigated under conditions (e.g. pH) outside the physiological range. The aim of the work presented in this thesis was to test the hypothesis that GO and MG are pro-oxidant and pro-inflammatory at (patho)physiological concentrations in both monocytes and pancreatic β-cells. In this work several new and important observations have been made regarding the action of α-dicarbonyls on oxidative stress and inflammation. 1) The amount of oxidative species production by α-dicarbonyls in glycation reactions with amino acids and proteins may be so low as to be negligible in vivo, despite previous evidence to the contrary. 2) α-dicarbonyls did not appear to generate oxidative stress within inflammatory cells nor pancreatic β-cells by depleting the levels of GSH. 3) At least in the β-cell model, the mechanism of action of the α-dicarbonyls did not involve dysregulation of the antioxidant SOD enzymes. 4) Neither α-dicarbonyl significantly affected insulin production by β-cells, except at cytotoxic concentrations. 5) Treatment of inflammatory cells with α-dicarbonyls induced release of the proinflammatory cytokine IL-8. 6) In both immune cells and pancreatic β-cells, α-dicarbonyls were involved in O2.- generation by activation and/or upregulation of NADPH oxidase. 7) Despite the structural similarities of α-dicarbonyls, they have distinct mechanisms of action with respect to oxidative stress.
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Rosa, Camila Moreno [UNESP]. "Influência do diabetes mellitus no coração de ratos senescentes espontaneamente hipertensos." Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/88563.
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As doenças cardiovasculares (DCV) são responsáveis por alta taxa de morbidade e mortalidade, tanto em países desenvolvidos como em desenvolvimento e, com o envelhecimento da população, a prevalência de seus fatores de risco está aumentando em ritmo alarmante. A hipertensão arterial sistêmica (HA5) e o diabetes mellitus (DM) estão entre os principais fatores de risco para o desenvolvimento das DCVe, quando associados, aumentam o risco de lesões orgânicas e morte cardiovascular. No entanto, poucos estudos têm analisado a influência do DM sobre o coração de portadores de HA5, e os resultados são controversos. Além disso, não é do nosso conhecimento estudos experimentais no modelo de DM em animais idosos. Considerando essas questões, o objetivo foi analisar a influência do DM sobre a remodelação ventricular e o estresse oxidativo em ratos senescentes espontaneamente hipertensos. Ratos espontâneamente hipertensos (5 HR), machos, com 18 meses de idade, foram divididos em dois grupos: 5HR-Controle (5HR-CTL, n=30) e 5HR-Diabético (5HR-DM, n=50). O DM foi induzido por meio de administração intraperitoneal de estreptozotocina (4-0 mg(kg). O consumo diário de ração e água e o peso corpóreo semanal foram medidos. A avaliação estrutural e funcional in vivo do coração foi realizada por meio do ecocardiograma. O estudo funcional in vitro foi realizado pela técnica do músculo papilar do ventrículo esquerdo (VE). Para análise estrutural in vitro, foram medidos os pesos do VE, ventrículo direito e átrios. Amostras dessas estruturas, do fígado e do pulmão foram utilizadas para o cálculo da razão peso úmido(peso seco desses órgãos. Amostras do VE foram obtidas para medir o diâmetro dos miócitos, a área ocupada pelo colágeno e a concentração de hidroxiprolina. O estresse oxidativo foi avaliado pela dosagem da concentração...
Cardiovascular diseases (CVD) are responsible for high morbidity and mortality rate in both developed and developing countries. with the population aging, the prevalence of CVD risk factors is increasing at alarming rate. Arterial hypertension (AH) and diabetes mellitus (DM) are major risk factors for development of CVD, and when combined increase the risk of organ damage and cardiovascular death. However, few studies have examined the inf1uence of diabetes on the heart of hypertensive patients, and the results are controversial. Moreover, to the best of our knowledge, there is no study in the animal model of DMin the elderly. Therefore, the aim of this study was to analyze the inf1uence of diabetes on ventricular remodeling and oxidative stress m senescent spontaneously hypertensive rats. Methods: Eighteen-month old male spontaneously hypertensive rats (SHR) were divided into two groups: SHR-Control (5HR-CTL, n==30) and SHR-Diabetic (SHR-DM, n==50). DM was induced by intraperitoneal administration of streptozotocin (40 mg(kg). Daily consumption of food and water and weekly body weight were measured. In vivo cardiac structural and functional parameters were measured by echocardiography. In vitro myocardial function was analyzed in left ventricular (LV) papillary muscles. LV,right ventricle, and atria weights were measured. Samples of these structures, liver, and lung were used to calculate the wetfdry weight ratio. LV samples were obtained to measure myocyte diameters, collagen fractional area, and hydroxyproline concentration. Oxidative stress was assessed by measuring lipid hydroperoxide concentration and superoxide dismutase and glutathione peroxidase activities, in LV tissue and serum. Comparisons between groups were performed by unpaired Student's t test 01' Mann-whítney test, according to normal 01' non-normal distribution, respectively... (Complete abstract click electronic access below)
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Cederberg, Jonas. "Oxidative stress, antioxidative defence and outcome of gestation in experimental diabetic pregnancy." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4960-3/.
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Inkster, Melanie E. "Development of vascular dysfunction in experimental diabetes : role of oxidative stress, angiotensin II and lipids." Thesis, University of Aberdeen, 2002. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU160140.
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The mesenteric vascular bed from the streptozotocin (STZ) diabetic model was used in this thesis to elucidate the mechanisms underlying diabetic vascular dysfunction. Treatment strategies targeting oxygen free radicals, angiotensin II, and lipids were investigated. In phenylephrine-preconstricted preparations, maximum vasodilation to acetylcholine, progressively deteriorated over 8 weeks of diabetes both before and after NO synthase inhibition which isolated the EDHF component. Chronic preventive treatment with silymarin, a free radical scavenger, or allopurinol, a xanthine oxidase inhibitor, partially protected against the development of 4-week diabetic deficits of the NO and EDHF systems. On the other hand, treatment with the semicarbizide-sensitive amine oxidase (SSAO) inhibitor, MDL74972A, only significantly improved the NO component. Preventive treatment with the transition metal chelator, trientine, produced significant protection of the NO and EDHF responses. Furthermore, intervention treatment not only protected against the development of an 8-week but also reversed some of the 4-week diabetic deficit. Both preventative and intervention treatments targeting angiotensin II production through either angiotensin-converting enzyme (ACE) inhibition with lisinopril or AT1 receptor blockade with candesartan provided some protection against the diabetic-induced decline in acetylcholine relaxations. Most notably, candesartan preventive treatment completely protected against a deficit in the EDHF response. Preventive treatment with rosuvastatin, a lipid-lowering drug, partially protected against the development of NO and EDHF deficits. The results show that experimental diabetes had deleterious effects on NO and EDHF-mediated vasodilation and suggest a role for free radicals, angiotensin II and lipids in this dysfunction.
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Leung, Joanne Yuen Ting. "Cardiovascular function in rat models of diabetes – the roles of hyperglycemia, inflammation and oxidative stress." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52724.
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Diabetes increases the risk of cardiovascular disease and mortality in humans. Although many diabetes-related studies have been conducted in recent years, the underlying pathogenesis still remains unclear. The aim of this thesis was to investigate if vascular and cardiac contractile dysfunction in rat models of streptozotocin-induced type 1 and fructose-streptozotocin-induced type 2 diabetes are associated with hyperglycemia, inflammation and oxidative stress, as these factors have been linked to the development of cardiovascular abnormalities in diabetes. Cardiovascular function was assessed via measurements of blood pressure, venous tone, vascular resistance, heart rate, cardiac contractility and cardiac index in vivo in diabetic as well as control rats. Moreover, these variables were evaluated following treatment with phlorizin (a glucose lowering agent), nimesulide (a selective inhibitor of cyclooxygenase-2) or N-acetylcysteine (an antioxidant). The results showed that arterial, venous and cardiac contractile responses to noradrenaline, adrenaline and/or dobutamine were depressed, to similar extents, in both models of diabetes relative to control animals, even though the rats with fructose-streptozotocin-induced diabetes had significantly higher plasma triglyceride levels than those with streptozotocin-induced diabetes. Administration of phlorizin, nimesulide and N-acetylcysteine did not affect any of the cardiovascular variables in the control rats, but significantly improved certain vascular and/or cardiac contractile responses in the diabetic rats. Specifically, α-adrenoceptor-mediated venous constriction was augmented by phlorizin in both rat models of diabetes, whereas arterial constriction remained attenuated. Acute administration of nimesulide did not alter cardiac contractile responses, but partially restored the venous and, to a less extent, arterial constriction in the diabetic rats, while chronic treatment with N-acetylcysteine ameliorated the arterial, venous as well as cardiac contractile functions. Collectively, these results suggest that the presence of hypertriglyceridemia does not significantly worsen in vivo cardiovascular function in our fructose-streptozotocin-induced rat model of type 2 diabetes, and demonstrate that hyperglycemia, inflammation and oxidative stress are, at least in part, implicated in diabetes-associated cardiovascular contractile dysfunction. Our studies have provided valuable insights into specific benefits of targeting hyperglycemia, inflammation and oxidative stress in the management of cardiovascular complications in type 1 and type 2 diabetes.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Alkazemi, Dalal Usamah Zaid. "Modulating factors of serum oxysterol concentrations in daughters from gestational diabetes and non-gestational diabetes." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100757.
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Pregestational and gestational diabetes (GDM) places the mother and her offspring at an increased risk for later development of insulin resistance and type 2 diabetes. Oxidative stress may mediate long-term disturbances in glucose homeostasis associated with type 2 diabetes and the metabolic syndrome. This thesis describes a cross-sectional study examining serum concentrations of free radical generated oxysterols as markers of oxidative stress in a cohort of teenage daughters from pregnancies with and without GDM. Daughters of GDM-pregnancies had a tendency of higher levels of serum oxysterols (7beta-hydroxycholesterol); however, this difference was not statistically significant after adjustment for total cholesterol. Serum oxysterols were significantly correlated with obesity measures such as waist circumference and BMI, which likely accounted for the tendency for higher measures of oxysterol concentrations in the GDM daughters. Oxysterols represent potentially important biomarkers for oxidative stress in adolescent girls as their levels track with the metabolic syndrome risk factors.Le diabète pré-gestationnel et le diabète de gestation (DG) augmentent le risque dedéveloppement d'une future résistance à l'insuline et de diabète de type 2 autant pourla mère que pour l'enfant. Le stress oxydatif est un facteur potentiel impliqué dans ledéséquilibre du glucose sanguin associé au diabète de type 2 et au syndromemétabolique. La présente thèse est une étude sectionnelle croisée, ayant pour but demesurer des marqueurs du stress oxidatif, notamment la concentration des oxystérolsgénérés par les radicaux libres dans le sérum d'adolescentes, nées de mères ayantprésenté ou non un diabète de gestation. Nos résultats montrent des concentrationsd'oxystérols (7P-hydroxycholesterol) plus élevées dans le sérum de filles issues degestations diabétiques à comparer aux filles de mères n'ayant pas eu de DG.Cependant, la différence entre les deux groupes n'était pas statistiquementsignificative après un ajustement au cholestérol total. La concentration d'oxystérolsétait significativement corrélée aux marqueurs d'obésité, notamment la circonférencede la taille et l'index de masse corporelle, possiblement à l'origine de la tendance desoxystérols à être plus élevés dans le cas des adolescentes issues de gestationsdiabétiques.
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Aljwaid, Husam O. Dakhil. "Relationships between iron, oxidative stress, glycated proteins and the development of atherosclerosis in Type 2 diabetes." Thesis, University of Plymouth, 2015. http://hdl.handle.net/10026.1/3222.
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Hyperglycaemia stimulates a variety of biochemical abnormalities. The area of particular interest in this study is the influence of non-enzymatic glycation of proteins on iron homeostasis, and particularly on non-transferrin-bound iron (NTBI) and its possible relation to atherogenesis in both Type 2 diabetic and obese non diabetic subjects. The link between non-enzymatic glycation of proteins and iron homeostasis, and development of macrovascular disease may be mechanistically different in Type 2 diabetic and obese non diabetic subjects due to a difference in the protein glycation pattern. Because the following in vivo study required storage of samples for up to two years to complete the processing of all the samples, a storage study was carried out using different anticoagulants and addition of reduced glutathione (GSH) to samples to study the effects of storage, thawing and freezing of the samples on the level of malondialdehyde (MDA), a biomarker of lipid peroxidation. This storage study showed that EDTA attenuated the action of lipid oxidation compared with lithium heparin (LiH). A combination of GSH with either EDTA or LiH added more protection from lipid peroxidation in the first week of storage, but due to the thawing and freezing of the sample the action of GSH diminished through its autooxidation, meaning that addition of GSH to samples in the following in vivo study would be useless. An in vivo study was carried out on iron-related parameters in three subject groups: control (non-diabetic, non-obese), Type 2 diabetic and obese non diabetic. Glycated haemoglobin (HbA1C) was strongly correlated with NTBI in the diabetic group. Also the level of NTBI was significantly increased in Type 2 diabetic subjects compared with other groups while the level of total iron was significantly decreased. The study showed a strong positive correlation between NTBI and a biomarker of endothelium dysfunction (E-selectin) in all groups studied. Although it is not possible from the current data to know if there is a causal relationship between these two parameters, it remains a possibility that iron released from its binding sites could initiate oxidative damage to the endothelial cells and begin the process of atherogenesis. Positive correlation at the 90% confidence level between NTBI and a biomarker of inflammation, high sensitivity C-reactive protein, is another indicator in this study of a link between increases in NTBI, inflammation, endothelium dysfunction and atherosclerosis. This study also showed for first time that NTBI is present in higher levels in the plasma of obese subjects compared to controls despite the obese subjects having significantly lower total iron. An in vitro study found that glycation of transferrin half saturated with iron increased with increasing glucose concentration, leading to decreased capacity of transferrin to hold iron and increased release of free iron. Also co-incubation of transferrin half saturated with iron with low density lipoprotein (LDL) and glucose showed oxidation of LDL (measured as MDA). This may be explained by the effect of glycation, leading to release of free iron, which catalyses oxidation of LDL. In addition, glycation of LDL may enhance the oxidation of LDL catalysed by iron. Both studies indicate that the glycation of proteins has a major impact on iron homeostasis leading to release of non-enzymatic glycation and contributing to one of the most common complications of Type 2 diabetes, atherosclerosis.
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Nash, Peppi. "Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7717.
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Impaired placentation and oxidative stress are proposed to play major roles in the pathogenesis of pre-eclampsia (PE). It has recently been pointed out that PE might be more than one disease and may have several different pathogeneses. This thesis describes a new animal model for PE and examines the role of oxidative stress in early respective late onset PE.
The effects of Suramin injections on day 10 and 11 of pregnancy were investigated in normal and diabetic rats of two strains (U and H), with or without additional vitamin E treatment. Suramin caused placental dysfunction in both rat strains: foetal growth restriction, increased resorption rate, reduced placental blood flow, and decreased maternal blood volume in the placenta. In the U strain Suramin also caused maternal hypertension and reduced renal blood flow. Oxidative stress in the Suramin treated rats was indicated by increased levels of isoprostane 8-iso-PGF2α in the placenta. Antioxidative treatment with vitamin E partly protected against the effects of Suramin. Streptozotocin-induced diabetes seemed to cause similar placental effects as Suramin, and in the diabetic rats the additional effects of Suramin were only moderate. In conclusion, Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction (U and H rats) and PE (U rats).
Oxidative stress was estimated in women with early onset (≤ 32 weeks) or late onset (≥ 35 weeks) PE, in normotensive pregnant women of respective gestational length, and in healthy non-pregnant women. The ratio of PAI-1/PAI-2 was measured in serum, and the amount of isoprostane 8-iso-PGF2α was measured in placenta, serum, and urine. The ratio of PAI-1/PAI-2 and placental isoprostane levels were higher in women with early onset PE compared with all other groups. Serum levels of isoprostane were similar between groups. Urinary levels of isoprostane were similar in all pregnant women, but lower in non-pregnant women. These data indicate that pregnancy increases general oxidative stress, and that early onset, but not late onset PE, causes increased oxidative stress also in placental tissue. The pathogeneses of early and late onset PE are, therefore, not likely to be identical.
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Du, Jing. "Anti-oxidative stress and Anti-inflammatory effects of atorvastatin improve endothelial dysfunction in experimental diabetes Mellitus." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2005/147/index.html.
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Sharma, G. "Methods for the measurement of urinary biomarkers of oxidative stress application to type 1 diabetes mellitus." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1344091/.
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The principal aim of the study was to develop methods for the measurement of potential urinary biomarkers of oxidative stress using liquid chromatography/tandem mass spectrometry with minimum sample preparation to avoid artefact formation. Initially the development of an assay to measure the urinary concentrations of isoprostanes (8- isoPGF2α) was attempted but this did not prove to be sufficiently sensitive and gave nonreproducible results. An assay to measure the intact sulphate and glucuronide conjugates of urinary metabolites of vitamin E [α-tocopheronolactone (α-TLHQ) and α-carboxy-ethylhydroxychroman (α-CEHC)] was then developed, as it has been suggested that α-TLHQ with an oxidised chroman ring might be an indicator of oxidative stress. A novel method was also developed to quantitate urinary amino acids associated with NO• metabolism (Larginine - precursor, L-citrulline - product, L-ADMA –inhibitor of nitric oxide synthase and L-homocysteine – reduces bioavailability of nitric oxide). This method was extended to quantitate seven additional amino acids. The latter two methods were applied to 32 children with type 1 diabetes and compared with age and sex matched controls. The mean concentrations of all the α-THLQ conjugates were highly significantly increased in the diabetic subjects (p<0.002). The concentrations of the α-CEHC conjugates were also increased but not to the same degree of significance (p<0.05). When the diabetic children were divided into those who were poorly (n=24) and adequately (n=8) controlled, the α- THLQ conjugates remained highly significantly increased (p<0.002) in the poorly controlled group compared to controls. However, the concentrations of the α-CEHC conjugates were not significantly different. The diabetic subjects had a highly significantly increased concentration (p<0.0001) of all the urinary amino acids studied compared to controls. These results suggest that the measurement of urinary α-TLHQ conjugates may provide a useful biomarker of oxidative stress. The clinical relevance of the increased concentrations of urinary amino acids in children with type 1 diabetes requires further investigation.
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Tahrani, Abd Al Magid. "Microvascular complications in patients with type 2 diabetes : the impact of ethnicity, sleep and oxidative stress." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4241/.
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Background: Diabetes-related Microvascular complications are associated with significant morbidity, mortality and economic burden. Effective treatments for microvascular complications, apart from improved metabolic and blood pressure control, are lacking. Hence, improved understanding of the pathogenesis of these complications is needed to develop new treatments. Obstructive sleep apnoea (OSA) is very common in type 2 diabetes (T2DM) and has been shown to stimulate the same harmful pathways as hyperglycaemia, particularly those that are involved in the pathogenesis of microvascular complications. Hence, it is plausible that OSA is associated with microvascular complications in patients withT2DM. Aims: To explore the interrelationships between OSA and microvascular complications in patients with T2DM and the possible mechanisms behind such relationship. Methods: A cross-sectional study of South Asians and White Europeans with T2DM were randomly recruited from the outpatients of two secondary care diabetes clinics in the UK. Patients were extensively characterised including assessments for OSA and microvascular complications. Results: Patients (n=234) were included in the analysis. OSA prevalence was 64.5%. OSA patients had worse metabolic profile than those without OSA. The prevalence of all microvascular complications (except cardiac autonomic neuropathy) was higher in patients with OSA compared to patients without. After adjustment for a wide range of confounders, OSA remained independently associated with microvascular complications. OSA and hypoxaemia severity correlated with the severity of complications. Based on blood samples and skin biopsies collected during the study, patients with OSA had increased oxidative and nitrosative stress and impaired microvascular regulation compared with patients without OSA. Furthermore, ethnic differences in OSA accounted for some of the ethnic differences in microvascular complications. Conclusion: I have identified a novel association between OSA and microvascular complications in patients with T2DM, with increased nitrosative stress and oxidative stress and impaired microvascular regulation as possible mechanisms. Further prospective observational and interventional studies are needed to assess the impact of OSA and its treatment on the development and progression of microvascular complications.
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Rosa, Camila Moreno. "Influência do diabetes mellitus no coração de ratos senescentes espontaneamente hipertensos /." Botucatu : [s.n.], 2011. http://hdl.handle.net/11449/88563.
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Resumo: As doenças cardiovasculares (DCV) são responsáveis por alta taxa de morbidade e mortalidade, tanto em países desenvolvidos como em desenvolvimento e, com o envelhecimento da população, a prevalência de seus fatores de risco está aumentando em ritmo alarmante. A hipertensão arterial sistêmica (HA5) e o diabetes mellitus (DM) estão entre os principais fatores de risco para o desenvolvimento das DCVe, quando associados, aumentam o risco de lesões orgânicas e morte cardiovascular. No entanto, poucos estudos têm analisado a influência do DM sobre o coração de portadores de HA5, e os resultados são controversos. Além disso, não é do nosso conhecimento estudos experimentais no modelo de DM em animais idosos. Considerando essas questões, o objetivo foi analisar a influência do DM sobre a remodelação ventricular e o estresse oxidativo em ratos senescentes espontaneamente hipertensos. Ratos espontâneamente hipertensos (5 HR), machos, com 18 meses de idade, foram divididos em dois grupos: 5HR-Controle (5HR-CTL, n=30) e 5HR-Diabético (5HR-DM, n=50). O DM foi induzido por meio de administração intraperitoneal de estreptozotocina (4-0 mg(kg). O consumo diário de ração e água e o peso corpóreo semanal foram medidos. A avaliação estrutural e funcional in vivo do coração foi realizada por meio do ecocardiograma. O estudo funcional in vitro foi realizado pela técnica do músculo papilar do ventrículo esquerdo (VE). Para análise estrutural in vitro, foram medidos os pesos do VE, ventrículo direito e átrios. Amostras dessas estruturas, do fígado e do pulmão foram utilizadas para o cálculo da razão peso úmido(peso seco desses órgãos. Amostras do VE foram obtidas para medir o diâmetro dos miócitos, a área ocupada pelo colágeno e a concentração de hidroxiprolina. O estresse oxidativo foi avaliado pela dosagem da concentração... (Resumo completo, clicar acesso eletrônico abaixo)Abstract: Cardiovascular diseases (CVD) are responsible for high morbidity and mortality rate in both developed and developing countries. with the population aging, the prevalence of CVD risk factors is increasing at alarming rate. Arterial hypertension (AH) and diabetes mellitus (DM) are major risk factors for development of CVD, and when combined increase the risk of organ damage and cardiovascular death. However, few studies have examined the inf1uence of diabetes on the heart of hypertensive patients, and the results are controversial. Moreover, to the best of our knowledge, there is no study in the animal model of DMin the elderly. Therefore, the aim of this study was to analyze the inf1uence of diabetes on ventricular remodeling and oxidative stress m senescent spontaneously hypertensive rats. Methods: Eighteen-month old male spontaneously hypertensive rats (SHR) were divided into two groups: SHR-Control (5HR-CTL, n==30) and SHR-Diabetic (SHR-DM, n==50). DM was induced by intraperitoneal administration of streptozotocin (40 mg(kg). Daily consumption of food and water and weekly body weight were measured. In vivo cardiac structural and functional parameters were measured by echocardiography. In vitro myocardial function was analyzed in left ventricular (LV) papillary muscles. LV,right ventricle, and atria weights were measured. Samples of these structures, liver, and lung were used to calculate the wetfdry weight ratio. LV samples were obtained to measure myocyte diameters, collagen fractional area, and hydroxyproline concentration. Oxidative stress was assessed by measuring lipid hydroperoxide concentration and superoxide dismutase and glutathione peroxidase activities, in LV tissue and serum. Comparisons between groups were performed by unpaired Student's t test 01'" Mann-whítney test, according to normal 01'" non-normal distribution, respectively... (Complete abstract click electronic access below)
Orientador: Katashi Okoshi
Coorientador: Ana Angélica Henrique Fernandes
Banca: Silméia Garcia Zanati
Banca: André dos Santos Moro
Mestre
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Gimenes, Camila [UNESP]. "Influência do exercício físico sobre a remodelaçao cardíaca e a atividade oxidativa em ratos diabéticos." Universidade Estadual Paulista (UNESP), 2012. http://hdl.handle.net/11449/100939.
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O Diabetes mellitus (DM) é um distúrbio caracterizado por resposta secretória inadequada de insulina, que se manifesta pela utilização inapropriada de glicose pelos tecidos com consequente hiperglicemia. Além das alterações cardíacas e vasculares, o DM pode acarretar doença miocárdica não aterogênica, denominada miocardiopatia diabética. Um dos principais mecanismos desencadeadores de alterações miocárdicas é o aumento na produção de espécies reativas de oxigênio (ERO). Na prevenção das complicações crônicas do DM, o exercício físico (EF) regular tem papel fundamental. Em estudos experimentais, ratos com DM induzido por estreptozotocina (STZ) e submetidos à EF têm apresentado melhora na homeostase miocárdica de glicose e da função cardíaca. O objetivo do presente trabalho foi avaliar a influência do EF sobre remodelação cardíaca, variáveis bioquímicas e atividade oxidativa em ratos diabéticos. Foram utilizados ratos Wistar divididos em quatro grupos: 1) controle sedentário (CS, n=14); 2) controle treinado (CT, n=13); 3) diabético sedentário (DS, n=19); e 4) diabético treinado (DT, n=18). O diabetes foi induzido por STZ e o protocolo de EF foi aplicado durante nove semanas. A avaliação estrutural e funcional in vivo do ventrículo esquerdo (VE) foi realizada por ecocardiograma. O estudo funcional in vitro foi realizado pela avaliação do músculo papilar do VE. Para análise de variáveis anatômicas foram medidos os pesos úmidos e secos do VE, ventrículo direito, átrios e amostras de fígado e pulmão. Amostras do VE foram utilizadas para medidas do diâmetro dos miócitos, do colágeno miocárdico e da concentração de hidroxiprolina. O estresse oxidativo miocárdico foi avaliado pela dosagem de hidroperóxido de lipídio (LOOH)...
Diabetes mellitus (DM) is a disorder characterized by inadequate insulin secretory response, manifested by inappropriate use of glucose by tissues with consequent hyperglycemia. In addition to cardiac and vascular changes, DM can cause a non-atherogenic myocardial disease, named diabetic cardiomyopathy. One of the main mechanisms responsible for myocardial changes is the increased production of reactive oxygen species (ROS). Physical exercise (PE) plays an important role in preventing diabetes chronic complications. In experimental studies, rats with streptozotocin (STZ)-induced diabetes subjected to PE have shown improved myocardial glucose homeostasis and cardiac function. The aim of this study was to evaluate the influence of PE on cardiac remodeling, biochemical variables, and oxidative stress in diabetic rats. Wistar rats were divided into four groups: 1) sedentary control (SC, n=14); 2) trained control (TC, n=13); 3) sedentary diabetic (SD, n=19); and 4) trained diabetic (TD, n=18). Diabetes was induced by STZ and PE protocol was applied for nine weeks. The in vivo cardiac structures and left ventricular (LV) function were assessed by echocardiography. The in vitro myocardial function was evaluated in LV papillary muscle preparation. For anatomical variables analysis, wet and dry weights of LV, right ventricle, atria, and samples of liver and lung were measured. LV samples were used for myocytes diameter, myocardial collagen and hydroxyproline measurements. The myocardial oxidative stress was assessed by measuring lipid hydroperoxide (LOOH), superoxide dismutase (SOD), glutathione peroxidase (GPH-Px), and catalase. Serum glucose, total cholesterol, HDL-cholesterol, and triglycerides were measured. At the end of the experiment, body weight (BW) was lower and glycemia higher in... (Complete abstract click electronic access below)
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Colbert, Kathryn Eileen. "Influence of dietary starches differing in glycemic index on pro-oxidant and anti-oxidant gene expression and insulin sensitivity in a mouse model." Auburn, Ala., 2007. http://repo.lib.auburn.edu/07M%20Theses/COLBERT_KATHRYN_13.pdf.
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White, Desley Louise. "Non-transferrin-bound iron and protein glycation in type 2 diabetes." Thesis, University of Plymouth, 2012. http://hdl.handle.net/10026.1/1181.
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Background and Methods: The involvement of iron in the risk for, and complications of, type 2 diabetes has generated substantial interest over the past 15 years, initially sparked by an association with raised serum ferritin, and the observation that people with iron overload diseases frequently develop diabetes. Considerable advances have since been made in understanding the effect glucose has on molecules, cells, and tissues; and the role that oxidative stress plays in the development of the pathologies of long-term diabetes. Poorly liganded iron is potentially both a contributor to, and consequence of, these complications. In vitro experiments with glucose-incubated transferrin by earlier workers have demonstrated loss of function with increasing glycation, leading to the suggestion that the failure of this key iron-binding protein may contribute to diabetic pathology, via the presence of redox active non-transferrin-bound iron (NTBI). In vitro glycated transferrin is examined here by ultrafiltration, to assess loss of function and possible oxidative fragmentation. Mass spectrometry is used to identify a range of amino acid glycation sites on in vitro glycated transferrin for the first time. Finally, several groups have previously measured NTBI in people with diabetes, finding little agreement in results. NTBI is measured here in a cohort of people with type 2 diabetes, using a new adaptation of earlier NTBI assays. NTBI is also assessed in pre-dialysis chronic kidney disease (CKD) stages I to III for the first time. Results and Conclusions: Experiments with glycated transferrin in vitro demonstrate oxidative fragmentation, explaining the loss of function reported by earlier groups. In vitro glycated transferrin examined by mass spectrometry reveals a substantial number and range of amino acids subject to glycation. Comparison with in vivo glycated transferrin suggests that many of the in vitro glycation sites are not glycated in vivo, and that there are many oxidized methionine residues which are potential artefacts, or likely to be repaired by methionine sulphoxide reductases in vivo. A study of people with type 2 diabetes finds no direct association between NTBI and protein glycation. Unexpected correlations between NTBI and LDL, and LDL and haemoglobin with increasing protein glycation, are reported for the first time. NTBI is suggested to be iron sourced from haemoglobin or haem, from erythrocyte haemolysis prior to sample collection. In people with pre-dialysis CKD stages I to III no significant difference in NTBI level compared to controls is seen, or correlations with markers of renal function. No link between NTBI and kidney function at this stage of disease is indicated.
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VanGilder, Reyna. "Examining the protective effects of sesamol on oxidative stress associated blood-brain barrier dysfunction in streptozotocin-induced diabetic rats." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10541.
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Thesis (Ph. D.)--West Virginia University, 2009.Title from document title page. Document formatted into pages; contains xi, 165 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 131-163).
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Gimenes, Camila. "Influência do exercício físico sobre a remodelaçao cardíaca e a atividade oxidativa em ratos diabéticos /." Botucatu, 2012. http://hdl.handle.net/11449/100939.
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Orientador: Katashi OkoshiCoorientador: Ana Angélica Henrique Fernandes
Banca: Wilson Nadruz Junior
Banca: André dos Santos Moro
Banca: Silmeia Garcia Zanati
Banca: Paula Schmidt Azevedo Gaiolla
Resumo: O Diabetes mellitus (DM) é um distúrbio caracterizado por resposta secretória inadequada de insulina, que se manifesta pela utilização inapropriada de glicose pelos tecidos com consequente hiperglicemia. Além das alterações cardíacas e vasculares, o DM pode acarretar doença miocárdica não aterogênica, denominada miocardiopatia diabética. Um dos principais mecanismos desencadeadores de alterações miocárdicas é o aumento na produção de espécies reativas de oxigênio (ERO). Na prevenção das complicações crônicas do DM, o exercício físico (EF) regular tem papel fundamental. Em estudos experimentais, ratos com DM induzido por estreptozotocina (STZ) e submetidos à EF têm apresentado melhora na homeostase miocárdica de glicose e da função cardíaca. O objetivo do presente trabalho foi avaliar a influência do EF sobre remodelação cardíaca, variáveis bioquímicas e atividade oxidativa em ratos diabéticos. Foram utilizados ratos Wistar divididos em quatro grupos: 1) controle sedentário (CS, n=14); 2) controle treinado (CT, n=13); 3) diabético sedentário (DS, n=19); e 4) diabético treinado (DT, n=18). O diabetes foi induzido por STZ e o protocolo de EF foi aplicado durante nove semanas. A avaliação estrutural e funcional in vivo do ventrículo esquerdo (VE) foi realizada por ecocardiograma. O estudo funcional in vitro foi realizado pela avaliação do músculo papilar do VE. Para análise de variáveis anatômicas foram medidos os pesos úmidos e secos do VE, ventrículo direito, átrios e amostras de fígado e pulmão. Amostras do VE foram utilizadas para medidas do diâmetro dos miócitos, do colágeno miocárdico e da concentração de hidroxiprolina. O estresse oxidativo miocárdico foi avaliado pela dosagem de hidroperóxido de lipídio (LOOH)... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Diabetes mellitus (DM) is a disorder characterized by inadequate insulin secretory response, manifested by inappropriate use of glucose by tissues with consequent hyperglycemia. In addition to cardiac and vascular changes, DM can cause a non-atherogenic myocardial disease, named diabetic cardiomyopathy. One of the main mechanisms responsible for myocardial changes is the increased production of reactive oxygen species (ROS). Physical exercise (PE) plays an important role in preventing diabetes chronic complications. In experimental studies, rats with streptozotocin (STZ)-induced diabetes subjected to PE have shown improved myocardial glucose homeostasis and cardiac function. The aim of this study was to evaluate the influence of PE on cardiac remodeling, biochemical variables, and oxidative stress in diabetic rats. Wistar rats were divided into four groups: 1) sedentary control (SC, n=14); 2) trained control (TC, n=13); 3) sedentary diabetic (SD, n=19); and 4) trained diabetic (TD, n=18). Diabetes was induced by STZ and PE protocol was applied for nine weeks. The in vivo cardiac structures and left ventricular (LV) function were assessed by echocardiography. The in vitro myocardial function was evaluated in LV papillary muscle preparation. For anatomical variables analysis, wet and dry weights of LV, right ventricle, atria, and samples of liver and lung were measured. LV samples were used for myocytes diameter, myocardial collagen and hydroxyproline measurements. The myocardial oxidative stress was assessed by measuring lipid hydroperoxide (LOOH), superoxide dismutase (SOD), glutathione peroxidase (GPH-Px), and catalase. Serum glucose, total cholesterol, HDL-cholesterol, and triglycerides were measured. At the end of the experiment, body weight (BW) was lower and glycemia higher in... (Complete abstract click electronic access below)
Doutor
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Clarke, Gregory B. "The effects of endurance exercise stress on the oxidative capacity of skeletal muscle of the streptozotocin diabetic rodent." Virtual Press, 1986. http://liblink.bsu.edu/uhtbin/catkey/475934.
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Young female Sprague-Dawley rats ( 50 gm., body weight-BW) were conditioned to treadmill activity (13.4 m•min -1; 0% grade) over a 12 d. period and then randomly assigned to groups combining exercise (E) and diabetes (D) with appropriate normal-sedentary controls (Sd). The diabetic condition was induced by I.V. injection of Streptozotocin (70 mg/kg BW) in citrate buffer and was evidenced by hyperglycemia (>330 mg. glucose/dl), polyuria and polydipsia. The E program was conducted 6 d./wk. Intensity and duration were progressively increased and reached 20% grade at 26.8 m•min-1 with 45 sec. sprints at 40.2 m-min-1 at 5 min. intervals. Total daily E time reached 60 min. for 8 wks. of training at which time experimental and appropriate control animals were sacrificed. Paramenters studied included in vitro capacity of slow oxidative (SO), fast oxidative. glycolytic (FOG), and fast glycolytic (FG) tissues to oxidize (Q02) pyruvate and palmitate. A 2x2 factorial ANOVA was used to detect E/Sd (Factor A) effects, D/non-D (Factor B) effects, and interaction (AxB) effects. A Student-Newman-Keuls multiple range test was employed to determine which experimental groups differed from each other. Results indicate a complex interaction of treatment effects depending upon muscle type. For the most part, E resulted in a reduction or modification of U effects. The DE group was not significantly different from either Sd or E controls for pyruvate 002 for all 3 muscle types. However, DS was significantly depressed below DE and controls for SO and FG tissues (pyruvate Q02). For palmitate 002 DE was significantly greater than both DSd and CSd groups for FOG tissue, (3244μ a 02/hr./gm vs. 2538 and 2555μl 02/hr/gm). Also both DE and CE were greater than both Sd groups for FG tissue (1925 and 1664μl 02/hr/gm vs. 1352 and 1283μ1 02/hr/gm, respectively). There were no significant differences between groups for SO tissue (palmitate Q02).
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Gimenes, Rodrigo [UNESP]. "Influência da inibição da NADPH oxidase sobre o redemodelamento cardíaco de ratos com diabetes mellitus." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/88566.
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000749048.pdf: 1237628 bytes, checksum: be3b98d2b93763097cb297cd0ce5e744 (MD5)O diabetes mellitus (DM) está associado a diversas doenças vasculares e cardíacas. Nos últimos anos, aumentaram as evidências de que pacientes diabéticos são acometidos por uma forma de doença miocárdica denominada miocardiopatia diabética. O aumento na produção de espécies reativas de oxigênio (EROs), causado por alterações metabólicas induzidas pelo DM, é um dos principais mecanismos desencadeadores de alterações miocárdicas. A maior fonte de EROs no sistema cardiovascular está relacionada a atividade da família de enzimas da NADPH oxidase. Em relação ao DM, há evidências de que a elevação da glicose sérica, induzida por estreptozotocina em camundongos ou em pacientes diabéticos, causa aumento na atividade da NADPH oxidase nos vasos. Sendo o sistema NADPH oxidase o principal responsável por desequilíbrio no sistema de produção e eliminação de EROs, e também por estar envolvido em muitas patologias cardíacas, estudos à respeito de seu bloqueio têm aumentado nos últimos anos. O objetivo do presente trabalho foi analisar a influência da inibição da NADPH oxidase por apocinina sobre o remodelamento cardíaco de ratos com DM. Foram utilizados ratos Wistar machos com 6 meses de idade, divididos em 4 grupos: controle (CTL, n=15), controle+apocinina (CTL+APO, n=20), diabético (DM, n=20) e diabético+apocinina (DM+APO, n=20). O diabetes foi induzido por estreptozotocina. Após 7 dias, foi iniciado tratamento com apocinina e mantido por 8 semanas. A avaliação estrutural e funcional in vivo do coração foi realizada por ecocardiograma. O estudo funcional in vitro foi realizado em músculo papilar isolado do ventrículo esquerdo (VE) em condições basal e após estimulação com manobras inotrópicas (contração pós-pausa, aumento da concentração extracelular de cálcio e adição de isoproterenol à solução nutriente). Para análise de variáveis anatômicas foram medidos os pesos úmidos...
Diabetes mellitus (DM) is associated with cardiac and vascular diseases. In recent years, there has been increased evidence that diabetic patients are affected by a form of myocardial disease known as diabetic cardiomyopathy. High production of reactive oxygen species (ROS), caused by diabetes-induced metabolic changes, is one of the main mechanisms leading to myocardial damage. A major source of ROS in the cardiovascular system is related to the activity of NADPH oxidase enzymes family. In streptozotocin-induced diabetic mice or in diabetic patients, serum glucose elevation increases NADPH oxidase activity in vessels. As NADPH oxidase is involved in imbalance of ROS production and elimination systems, and in pathophysiology of cardiac diseases, research on its blockade has increased in recent years. The purpose of this study was to analyze the influence of NADPH oxidase inhibition by apocynin on cardiac remodeling in rats with DM. Six month old male Wistar rats were assigned into 4 groups: control (CTL, n=15), control+apocynin (CTL+APO, n=20), diabetic (DM, n=20) and diabetic+apocynin (DM+APO, n=20). Diabetes was induced by streptozotocin. Seven days later, apocynin was initiated and maintained for 8 weeks. In vivo cardiac structures and functions were assessed by echocardiography. In vitro left ventricular (LV) functional study was performed in isolated papillary muscle preparation at basal condition and after inotropic stimulation with post-rest contraction, increase of extracellular calcium concentration, and addition of isoproterenol to the nutrient solution. Wet and dry weights of LV, right ventricle (RV), atria, lung, and liver sample were measured. LV histological sections were used to analyze interstitial collagen fraction. Antioxidant enzymes glutathione peroxidase (GSH-Px), catalase, and superoxide dismutase (SOD) were measured in serum. LV tissue samples were obtained for determination of ...
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Chung, Wai Shing. "Investigation on the correlation between redox changes and oxidative stress in diabetes, and their role in transcription factors activation in vitro and in vivo." HKBU Institutional Repository, 2002. http://repository.hkbu.edu.hk/etd_ra/428.
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Haeser, Alexsandro da Silva. "O Estresse oxidativo e a depressão no diabetes em modelo animal : o efeito do clonazepam." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2006. http://hdl.handle.net/10183/10451.
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Objetivo: o presente estudo teve como objetivo avaliar o estresse oxidativo em animais diabéticos e não diabéticos submetidos ao modelo experimental de depressão, o nado forçado, e os efeitos do clonazepam, um modulador positivo GABAA, correlacionado os efeitos comportamentais com as alterações bioquímicas. Metodologia: ratos Wistar machos com 30 dias de idade, foram induzidos ao Diabetes por estreptozotocina e submetidos ao teste de natação forçada 21 dias após a indução. Após uma ambientação, o clonazepam foi administrado na dose 0,5 mg/Kg, bem como solução salina nos controles, 24, 5 e 1 hora antes do teste. A freqüência e a duração dos comportamentos neste teste foi registrada em vídeo cassete para avaliação etológica dos comportamentos por pesquisador treinado. Trinta minutos após o teste, os animais foram sacrificados por decapitação e foram separados o plasma e os eritrócitos, bem como os tecidos cerebrais córtex pré-frontal, estriado e hipocampo. Foram avaliadas as espécies reativas ao ácido tiobarbitúrico (TBARS) e a reatividade antioxidante total (TAR), bem como a atividade das enzimas antioxidantes catalase (CAT) e superóxido dismutase (SOD). Resultados e discussão: os resultados mostraram um aumento significativo do TBARS e uma diminuição significativa do TAR no plasma de animais diabéticos, efeitos estes revertidos pelo clonazepam. Não houve alteração na atividade da SOD e da CAT em eritrócitos. No hipocampo observou-se um aumento significativo no TBARS nos diabéticos, também revertido pelo clonazepam, sendo que nenhuma alteração foi verificada na medida do TAR. O aumento significativo do TBARS no córtex de ratos diabéticos, um indicador de lipoperoxidação, e a diminuição significativa do TAR no córtex dos animais diabéticos, um indicador da capacidade de modulação da ação dos radicais livres produzidos, não foram revertidos pela administração do clonazepam neste tecido cerebral. Ainda, não houve alteração do TBARS e do TAR no estriado dos grupos testados. O clonazepam foi capaz de reverter a imobilidade dos animais diabéticos submetidos ao teste de natação forçada. Não foi verificada correlação significativa entre a imobilidade e as medidas de TBARS e TAR. Conclusão: considerando a conhecida ação ansiolítica e antidepressiva do clonazepam, sugere-se que ele possa ser uma alternativa terapêutica na depressão em pacientes diabéticos, uma vez que ele não altera a glicemia e, pelos resultados aqui apresentados, teria uma ação protetora contra os radicais livres, os quais sabidamente contribuem para o desenvolvimento das complicações secundárias de Diabete Mellitus.Objective: the present study had as objective to evaluate the oxidative stress from diabetic animals submitted to an experimental model of depression (forced swimming) and the effects of clonazepan, a GABA agonist, correlating behavioral with biochemical effects. Methodology: male Wistar rats, 30 days years old, were induced to diabetes with streptozotocin and submitted to forced swimming test 21 days after induction. After to be accustomed with the environment, clonazepan was administered to rats in a dose of 0,5 mg/kg, as well as saline solution to control rats, 24, 5 and 1 hours before test. The frequency and duration of behaviour in the test were filmed for ethologic evaluation by a trained pearson. Thirty minutes after test, the animals were sacrified by decapitation, and plasma and erythrocytes were separated, as well as hippocamp, cortex and striatum. Reactive species of tiobarbituric acid (TBARS) and total antioxidant reactivity (TAR), as well as antioxidant enzyme activities catalase (CAT) and superoxide dismutase (SOD) were evaluated. Results and discussion: results showed a significant increase of TBARS and a significant decrease of TAR in plasma from diabetic animals, which was altered by clonazepan. There were no effect of CAT and SOD activities in erytrocytes from tested animals. The results observed in hippocamp showed a significative increase of TBARS from diabetics rats, inverted by clonazepan, and no one alteration was verified in TAR. The significant increase of TBARS in cortex from diabetic rats, an indicator of lipoperoxidation, and the significant decrease of TAR in cortex from diabetic rats, an indicator of modulation capability against free radicals, were not altered by clonazepan administration. Besides, there were no alteration of TBARS and TAR in striatum from tested animals. Clonazepan was capable to alter the immobility from diabetic animals submitted to forced swimming. There was no significative correlation between immobility and TBARS neither TAR measurements. Conclusion: considering the ansiolitic and antidepressive action of clonazepan, it’s suggested that it could be an alternative therapeutic for depression to diabetic patients, once clonazepan do not alter glycemia and, by the results here presented, could give a protection against free radicals, which are known to contribute to the development of complications in Mellitus Diabetes.
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Gobbo, Marina Guimarães 1987. "Influência da hiperglicemia e do estresse oxidativo na cinética de proliferação e morte celular no epitélio acinar da próstata de ratos diabéticos." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317898.
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Orientador: Rejane Maira GóesDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Os prejuízos do diabetes sobre a morfofisiologia prostática são conhecidos e associados à falta de insulina, queda de andrógenos e hiperglicemia. Estudos anteriores com diabetes mostraram ampla variação individual da resposta histológica da próstata frente a esta doença. Visando esclarecer os fatores responsáveis por essa variação, foram examinadas as correlações entre resposta histológica da próstata com a glicemia, com os níveis séricos de testosterona e estrógeno no diabetes em curto termo. Sabe-se que a hiperglicemia leva à formação de produtos finais de glicação não-enzimática (AGE) e à conseqüente superprodução de espécies reativas de oxigênio. Um aumento na apoptose foi constatado previamente no epitélio prostático após longos períodos de diabetes e da queda androgênica, sugerindo a influência da hiperglicemia e do estresse oxidativo nesse processo. Assim, no primeiro experimento, foi analisado o impacto do diabetes induzido por estreptozotocina no sistema antioxidante (AOS) da próstata ventral de ratos (VP) e a influência da suplementação com vitamina C (ácido ascórbico). Também foram examinadas as repercussões do estresse oxidativo na sensibilidade androgênica e cinética de proliferação e morte celular dessa glândula. Para isso, induziu-se o diabetes em ratos Wistar adultos pela estreptozotocina (4 mg/100g peso corporal), seguidos ou não do tratamento com vitamina C (150 mg/kg peso corporal/dia), via gavagem. Foram formados os seguintes grupos: controle (C), controle tratado com vitamina C (C+V), diabético (D) e diabético tratado com vitamina C (D+V). Os animais foram sacrificados após 30 dias de diabetes e a VP foi processada. Os níveis de malondialdeído (MDA) e as atividades de catalase (CAT), superoxido dismutase (SOD), glutationa peroxidadase (GPx) e glutationa S-transferase (GST) foram mensurados na próstata e no sangue. A vitamina C diminuiu os níveis de apoptose elevados pelo diabetes, porém não normalizou a proliferação celular nem protegeu contra o dano oxidativo. O AOS sangüíneo não foi afetado com um mês de diabetes, porém os níveis de CAT e GST aumentaram na glândula. O MDA e a expressão de N?-(carboxymetil) lisina (CML), um dos principais AGE, também elevaram marginalmente nos grupos diabéticos. Também foi realizado um segundo experimento de indução do diabetes pela aloxana (42 mg/kg de peso corpóreo) com ou sem tratamento com insulina (5 UI/dia) As alterações morfológicas na VP foram examinadas em cortes histológicos em historresina, segundo as diferentes faixas de glicemia. Constatou-se uma relação inversa entre a glicemia e a razão testosterona/estrógeno com o peso da VP. A atrofia nas extremidades distais dos ductos mostrou-se associada com altos valores glicêmicos. A insulina não impediu as alterações causadas pelo diabetes, principalmente quando o controle da glicemia não foi eficaz. Deste modo, o dano oxidativo é responsável, parcialmente, pelo desequilíbrio na proliferação e morte celular causados pelo diabetes. A GST é um bom indicador da defesa antioxidante na próstata nos estágios iniciais dessa desordem metabólica e o aumento de sua atividade pode estar relacionado com o subseqüente desenvolvimento de lesões malignas. Nossos dados indicam que a hiperglicemia prolongada aliada ao desequilíbrio hormonal sejam os principais responsáveis pelas alterações drásticas na VP dos animais diabéticos sem reposição de insulina
Abstract: The diabetes damages in prostate morphophysiology are well known and are triggered by insulin lack, low androgen levels and hyperglycemia. Previous researches showed an individual variation in morphological prostate response against this disease. In order to clarify the factors responsible for this variation, we examined the correlation between histological response of the prostate with glycemia, serum testosterone and estrogen levels under short term diabetes. It is known that high glucose levels lead to the formation of end products of non-enzymatic glycation (AGE) and the subsequent overproduction of reactive oxygen species. An apoptosis increase was also reported in prostatic epithelium after long periods of diabetes and androgen drift, suggesting the influence of hyperglycemia and oxidative stress in this imbalance. The first experiment was performed to evaluate the impact of estreptozotocin-induced diabetes in the antioxidant system (AOS) of rat ventral prostate (VP) and the influence of supplementation with vitamin C (ascorbic acid). The effects of oxidative stress in androgen sensitivity and proliferation and cell death kinetics, in this gland, were also assessed. For this purpose, diabetes was induced in adult male rats by streptozotocin (4 mg/100g b.w) followed or not by treatment with vitamin C (150 mg/kg b.w./day), by gavage. The following groups were formed: control (C), control treated with vitamin C (C+V), diabetic (D) and diabetic treated with vitamin C (D+V). The animals were sacrificed after 30 days of diabetes onset and the VP was processed. The malondialdehyde levels (MDA) and catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities were measured in the prostate and blood. Vitamin C reduced the high apoptosis levels due to diabetes, but did not normalize cell proliferation and it was not totally efficient against oxidative damage. The blood AOS was unaffected by one month of diabetes, but the CAT and GST activities were increased in the gland. The MDA levels and N?-(carboxymetil) lysine (CML) expression, one of the main AGE, were marginally increased in diabetic groups. A second experiment of diabetes induction was based in alloxana induction (42 mg/kg b.w.) with or without insulin treatment. Morphological changes in the VP were examined in histological hystoresin sections, according to different ranges of glycemia. Glucose levels and testosterone/estrogen ratio were inversely related to the VP weight. The atrophy in the distal ends of prostate ducts was associated with high blood glucose levels. Insulin does not prevent the changes caused by diabetes, especially if glycemic control is not effective. These results suggest that oxidative damage is partly responsible for the imbalance in proliferation and cell death caused by diabetes. GST is a good indicator of prostate antioxidant defense in the early stages of this metabolic disturbance and its increased activity may be related to the malignant lesions establishment. Our data indicates that prolonged hyperglycemia combined with hormonal disequilibrium are the main responsible for the drastic changes in the VP of diabetic animals without insulin replacement
Mestrado
Biologia Celular
Mestre em Biologia Celular e Estrutural
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Gimenes, Rodrigo. "Influência da inibição da NADPH oxidase sobre o remodelamento cardíaco de ratos com diabetes mellitus /." Botucatu, 2013. http://hdl.handle.net/11449/88566.
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Orientador: Katashi OkoshiBanca: Paula Schmidt Azevedo Gaiolla
Banca: Fabio Fernandes
Resumo: O diabetes mellitus (DM) está associado a diversas doenças vasculares e cardíacas. Nos últimos anos, aumentaram as evidências de que pacientes diabéticos são acometidos por uma forma de doença miocárdica denominada miocardiopatia diabética. O aumento na produção de espécies reativas de oxigênio (EROs), causado por alterações metabólicas induzidas pelo DM, é um dos principais mecanismos desencadeadores de alterações miocárdicas. A maior fonte de EROs no sistema cardiovascular está relacionada a atividade da família de enzimas da NADPH oxidase. Em relação ao DM, há evidências de que a elevação da glicose sérica, induzida por estreptozotocina em camundongos ou em pacientes diabéticos, causa aumento na atividade da NADPH oxidase nos vasos. Sendo o sistema NADPH oxidase o principal responsável por desequilíbrio no sistema de produção e eliminação de EROs, e também por estar envolvido em muitas patologias cardíacas, estudos à respeito de seu bloqueio têm aumentado nos últimos anos. O objetivo do presente trabalho foi analisar a influência da inibição da NADPH oxidase por apocinina sobre o remodelamento cardíaco de ratos com DM. Foram utilizados ratos Wistar machos com 6 meses de idade, divididos em 4 grupos: controle (CTL, n=15), controle+apocinina (CTL+APO, n=20), diabético (DM, n=20) e diabético+apocinina (DM+APO, n=20). O diabetes foi induzido por estreptozotocina. Após 7 dias, foi iniciado tratamento com apocinina e mantido por 8 semanas. A avaliação estrutural e funcional in vivo do coração foi realizada por ecocardiograma. O estudo funcional in vitro foi realizado em músculo papilar isolado do ventrículo esquerdo (VE) em condições basal e após estimulação com manobras inotrópicas (contração pós-pausa, aumento da concentração extracelular de cálcio e adição de isoproterenol à solução nutriente). Para análise de variáveis anatômicas foram medidos os pesos úmidos ...
Abstract: Diabetes mellitus (DM) is associated with cardiac and vascular diseases. In recent years, there has been increased evidence that diabetic patients are affected by a form of myocardial disease known as diabetic cardiomyopathy. High production of reactive oxygen species (ROS), caused by diabetes-induced metabolic changes, is one of the main mechanisms leading to myocardial damage. A major source of ROS in the cardiovascular system is related to the activity of NADPH oxidase enzymes family. In streptozotocin-induced diabetic mice or in diabetic patients, serum glucose elevation increases NADPH oxidase activity in vessels. As NADPH oxidase is involved in imbalance of ROS production and elimination systems, and in pathophysiology of cardiac diseases, research on its blockade has increased in recent years. The purpose of this study was to analyze the influence of NADPH oxidase inhibition by apocynin on cardiac remodeling in rats with DM. Six month old male Wistar rats were assigned into 4 groups: control (CTL, n=15), control+apocynin (CTL+APO, n=20), diabetic (DM, n=20) and diabetic+apocynin (DM+APO, n=20). Diabetes was induced by streptozotocin. Seven days later, apocynin was initiated and maintained for 8 weeks. In vivo cardiac structures and functions were assessed by echocardiography. In vitro left ventricular (LV) functional study was performed in isolated papillary muscle preparation at basal condition and after inotropic stimulation with post-rest contraction, increase of extracellular calcium concentration, and addition of isoproterenol to the nutrient solution. Wet and dry weights of LV, right ventricle (RV), atria, lung, and liver sample were measured. LV histological sections were used to analyze interstitial collagen fraction. Antioxidant enzymes glutathione peroxidase (GSH-Px), catalase, and superoxide dismutase (SOD) were measured in serum. LV tissue samples were obtained for determination of ...
Mestre
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Kimzey, Michael John. "Identification, Characterization, and Quantification of Dicarbonyl Adducts in the Plasma Proteome in Type-2 Diabetes." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/145123.
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Glyco-oxidation is linked to the pathophysiology of diabetes and diabetic complications. The process of glyco-oxidation generates reactive dicarbonyls, which form adducts on arginine residues in distributions throughout the proteome that are site-specific depending on the protein microenvironment. Dicarbonyl adducts are thus markers for glyco-oxidative stress. Various approaches using mass spectrometry permits the identification, localization, and quantification of these dicarbonyl adducts. Using MG as a model dicarbonyl, a shotgun proteomics approach identified the sites for modification of major plasma proteins. Thirty five sites on seven abundant plasma proteins were found, and investigation into the microenvironment surrounding the target arginine sites revealed a neighboring charged residue motif where adjacent residues were either negatively or positively charged. One of the sites identified was R257 in HSA, which is located in the important drug binding site I. We validated drug site I as a target for MG modification by the adaptation of two assays to monitor the effect of MG modification. MG significantly decreases the rate of hydrolysis of PGE2 in drug site I, and induces the displacement of prodan from drug site I. Molecular modeling of warfarin docking at drug site I with the MG-modified R257 resulted in significantly decreased binding and change in binding orientation. The oxidation products of susceptible residues methionine, tryptophan, and cysteine were evaluated using MRM of oxidized HSA peptides. Oxidation of methionine gave the M+16 single oxidized product, and M329 in HSA was the most responsive site. Oxidation of the sole W214 tryptophan produced the W+32 double oxidation product, and oxidation of C34 produced the C+48 triple oxidation product. MG, 3DG, and glucosone were evaluated for propensity to modify 12 HSA sites based on MRM of dicarbonyl modified HSA. Dicarbonyl modification was independent of arginine solvent accessibility. In a clinical study using nephropathy as an endpoint, sites of oxidation and modification of HSA by MG, 3DG, and glucosone were quantified by MRM. The most important variable among diabetic subjects was metformin use, and subjects taking metformin had significantly reduced markers for glyco-oxidation. These findings may be useful in the development of new diabetes therapies that aim to ameliorate glyco-oxidative stress.
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Dias, Alexandre Simões. "O antioxidante quercetina diminui o estresse oxidativo hepático em ratos diabéticos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2005. http://hdl.handle.net/10183/8174.
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Introdução: O diabetes mellitus (DM) é uma doença que apresenta elevada incidência e prevalência na população em diversas partes do mundo, e, estudos experimentais e clínicos, sugerem que o estresse oxidativo esteja envolvido na patogênese e na progressão da mesma. Objetivo: Este estudo tem como objetivo investigar os efeitos do antioxidante quercetina administrado intraperitonealmente sobre o estresse oxidativo, a ativação do fator de transcrição nuclear kappa B (NF-kB) e expressão da óxido nítrico sintase induzível (iNOS) hepática no modelo experimental de DM tipo I. Material e métodos: Foram utilizados 32 ratos machos Wistar, divididos em quatro grupos de oito animais: controle, controle que receberam a quercetina, diabéticos não tratados e diabéticos tratados com quercetina. A dose utilizada da quercetina foi de 50 mg/Kg de peso corporal diariamente. O DM foi induzido por única injeção intraperitoneal de estreptozotocina (70 mg/kg). Após oito semanas (60 dias), foi avaliado os marcadores do estresse oxidativo hepático através das substâncias que reagem ao ácido tiobarbitúrico (TBARS), e a quimiluminescência (QL). A atividade hepática das enzimas antioxidantes catalase (CAT), superóxido dismutase (SOD) e glutationa peroxidase (GPx), bem como a ativação do NF-kB pelo método (Electrophoretic Mobility Shift Assay – EMSA) foram mensurados. Também foram avaliados a expressão das quinases dos inibidores do NF-kB (IKK-a e IKK-b), bem como os inibidores (IkB-a e IkB-b) e a iNOS hepática pela técnica do Wersten blot. Resultados: A concentração da glicose sangüínea aumentou significativamente nos animais diabéticos e não diminuiu após a administração da quercetina. No tecido hepático dos animais diabéticos aumentou o TBARS, a QL, a atividade da SOD e da CAT, e no grupo diabético que recebeu a quercetina os valores diminuíram. O DM aumentou a ativação do NF-kB, os níveis do IKK-a e da iNOS, e diminuiu o IkB-a. Todos os valores foram atenuados quando administrado a quercetina, somente a atividade da GPx, do IKK-b e IkB-b não apresentou diferença entre os grupos estudados. Conclusão: A quercetina inibiu o estresse oxidativo hepático, a ativação do NF-kB e a expressão da iNOS. O tratamento com o antioxidante quercetina parece inibir as vias sinalizadoras de transdução, podendo interferir na produção dos mediadores nóxios envolvidos no modelo experimental de DM.Introduction: Diabetes mellitus (DM) is an disease that presents high incidence and prevalence in the population in diverse parts of the world, and, experimental studies and clinical, suggest that oxidative stress is involved in pathogenesis and progression of the same. Objective: This study it has as objective to investigate the effect of quercetin treatment on oxidative stress, the activation of the factor of nuclear transcription kappa B (NF-kB) and hepatic expression of inducible nitric oxide sintase (iNOS) in the experimental model of DM type I. Material and methods: Male rats Wistar had been used, divided in four groups with eight animals: control, control that had received quercetin, diabetic not treated and diabetic treated with quercetin. The used dose of quercetin was of 50 mg/Kg of corporal weight intraperitoneally (i.p.) daily. The DM was induced for i.p. injection of estreptozotocin (70 mg/kg). After eight weeks (60 days), it was evaluated the markers of oxidative stress hepatic through the thiobarbituric acid reactive substances (TBARS), and the chemiluminiscence (QL). The hepatic activity of antioxidants enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), as well as the activation of the NF-kB for the method (Electrophoretic Mobility Shift Assay - EMSA) had been measured. Also they had been evaluated the expression of quinases of inhibitors of the NF-kB (IKK-a and IKK-b), as well as inhibitors (IkB-a and IkB-b) and iNOS for the Western blot. Results: Blood glucose concentration increased significantly in the diabetic animals and did not decreased after administration of quercetin. In hepatic tissue of diabetic animals increased the TBARS, the QL, the activity of the SOD and the CAT, and in the diabetic group that received the quercetin the values had diminished. The DM increased the activation of the NF-kB, the levels of the IKK-a and iNOS, and decreased the IkB-a. All the values had been attenuated when used the quercetin, only the activity of the GPx, the IKK-b and IkB-b did not present difference between the studied groups. Conclusion: The quercetin inhibited the hepatic oxidative stress, the activation of NF- kB and the expression of the iNOS. The treatment with the antioxidant quercetin seems to inhibit the signal transduction pathway, may block the production of noxios mediators involved in the experimental model of DM.
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Almeida, Maíra Estanislau Soares de. "Hiperglicemia e interação fibroblasto-matriz extracelular - influências na adesão e migração em substratos bidimensional e tridimensional." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-26012012-133459/.
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Diabetes mellitus (DM) é caracterizado pela hiperglicemia crônica (HG), responsável por diversas complicações de longo prazo, como por exemplo a cicatrização deficiente. Nós investigamos os efeitos da HG na migração de fibroblastos dérmicos sobre colágeno e fibronectina, utilizando substratos bidimensional (2-D) e tridimensional (3-D). Observamos que a HG reduziu a velocidade de migração em ambas as matrizes. O tratamento sistêmico com antioxidantes preveniu esses efeitos. A velocidade de formação das protrusões celulares não foi afetada, mas houve uma redução na estabilidade das mesmas, sugerindo comprometimento das adesões. De fato, a HG reduziu a adesão celular sobre colágeno e fibronectina, enquanto o espraiamento celular estava reduzido sobre o colágeno e aumentado sobre fibronectina. Adicionalmente, a distribuição das subunidades a1, av e a5 de integrinas foi afetada pela HG. Esse estudo mostrou que os efeitos da HG sobre a migração celular envolvem mecanismos básicos comuns a vários substratos, mas também mecanismos especificamente relacionados com a adesão à fibronectina, envolvendo possivelmente o estresse oxidativo e vias de sinalização iniciadas nas adesões.Diabetes mellitus (DM) is characterized by chronic hyperglycemia (HG), which causes several complications, including impaired wound healing. We investigated the effects of HG on the migration of primary dermal fibroblasts on collagen and fibronectin, using two-dimensional (2-D) and three-dimensional (3-D) substrates. We observed that HG reduced migration velocity on both matrices. Systemic treatment with antioxidants prevented these effects. The velocity of protrusion formation was unaffected, but a decrease in protrusion stability was observed. HG slightly interfered with cell adhesion on collagen and fibronectin, but cell spreading was reduced on collagen and increased on fibronectin. Accordingly, the distribution of the integrin subunits a1, av and a5 was affected by HG. This study shows that the effects of HG on cell migration involve basic mechanisms common to various substrates, as well as mechanisms specifically related to fibronectin, possibly involving oxidative stress and adhesion signaling.
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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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Kachepe, Prisca. "The possible therapeutic effects of vindoline on testicular and epididymal function in diabetes-induced oxidative stress male Wistar rats." Thesis, Cape Peninsula University of Technology, 2018. http://hdl.handle.net/20.500.11838/3084.
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Thesis (MSc (Biomedical Technology))--Cape Peninsula University of Technology, 2018Diabetes mellitus is defined as a group of metabolic disorders characterised by chronic hyperglycaemia due to insufficient production and/or action of insulin and is regarded as one of the major sources of morbidity, mortality and economic burden to the modern society. A large body of scientific evidence support the fact that oxidative stress is elevated in diabetic conditions. Oxidative stress plays a significant role in the development of secondary complications of diabetes including diabetes-linked male sexual dysfunction. The management of sexual dysfunction as a secondary complication of diabetes relies on the management of the underlying diabetic condition. Glycaemic control and increased antioxidant protection are therefore necessary in the management of diabetes-induced oxidative stress male infertility. Pharmacological management of diabetes in form of various antihyperglycaemic, synthetic drugs has improved the outlook of diabetic patients; however, they are expensive, harbour unfavourable adverse effects and some have done little to prevent secondary complications of diabetes including diabetes-induced male sexual dysfunction. In addition to this, access to basic technologies for the management of diabetes mellitus and its secondary complications is still a challenge in low resource areas. Because of these challenges, there is a need to search for alternative remedies such as medication from natural products which are more affordable, well tolerated by the human body and are easily accessible. Medicinal plants are therefore viewed as an easily accessible and potent source of antioxidants capable of scavenging free radicals and fighting diabetes-induced oxidative stress. This study therefore investigated the effects of vindoline; an alkaloid extractable from Cantharanthus roseus in ameliorating diabetes-induced oxidative stress effects in testicular and epididymal tissues using male Wistar rats. Forty-eight (48), 6-week old male Wistar rats weighing between 190-230g with a conventional microbial status were divided into 6 groups, n=8, and used for this research project. Group 1 was the normal control, group 2 comprised non-diabetic rats treated with vindoline, and group 3 was the non-diabetic group of rats treated with glibenclamide- the standard drug for the treatment of diabetes. Group 4 was the diabetic control, group 5 comprised diabetic rats treated with vindoline and group 6 was the diabetic group of rats treated with glibenclamide. Diabetes was induced in group 4, group 5 and group 6 rats by subjecting them to 10% fructose water over a period of 2 weeks and thereafter, administering a single intraperitoneal injection of 40 mg/kg b.w streptozotocin (STZ). Fasting blood glucose levels were measured 72 hours after STZ injection and hyperglycaemia was confirmed where fasting blood glucose levels were more than 18mmol/l. The diabetic control (group 4) had higher fasting blood glucose levels, lower body weights as well as lower testicular and epididymal weights in comparison to the normal control (group 1). Additionally, the extent of lipid peroxidation in testicular and epididymal tissues of the diabetic control (group 4) was higher in comparison to that of the normal control (group 1). The diabetic control had lower testicular and epididymal antioxidant enzyme activities (superoxide dismutase and catalase) and lower oxygen radical absorption capacity (ORAC) in comparison to the normal control. Ferric reducing antioxidant power (FRAP) in testicular and epididymal tissues of the diabetic control (group 4) were not significantly different from those of the normal control (group 1). Treatment of diabetic rats with vindoline (group 5) for 5 weeks significantly reduced fasting blood glucose levels although the extent of reduction could not restore diabetic blood glucose levels to near-normal levels. Overall, treatment of diabetic rats with vindoline was able to minimise testicular oxidative stress as reflected by reduction in testicular malondialdehyde (MDA) levels. Furthermore, results of this study showed an increase in both testicular and epididymal catalase activities, an increase in epididymal SOD, an increase in testicular ORAC as well as an increase in both testicular and epididymal FRAP levels after 5 weeks of treating diabetic rats with vindoline (group 5). Epididymal lipid peroxidation levels, epididymal ORAC levels and testicular SOD levels of diabetic rats treated with vindoline (group 5) were however not significantly different from those of the diabetic control (group 4). Treatment of diabetic rats with vindoline or glibenclamide could not restore total body weights and testicular weights of group 5 and group 6 rats respectively, to near-normal levels. Furthermore, epididymal weights and testicular SOD activity of diabetic rats treated with vindoline (group 5) were not significantly different from those of the normal control (group 1). In conclusion, findings from this study demonstrated that treatment with vindoline could have protective effects against diabetes-induced oxidative stress in both testicular and epididymal tissues of male Wistar rats. Vindoline can therefore be considered a potential agent for the management of diabetes-induced oxidative stress male sexual dysfunction. Further studies with advanced technologies are however recommended to study the possible efficacy of vindoline in ameliorating diabetes-induced oxidative stress male sexual dysfunction. Furthermore, studies on the dose-dependent effects and long-term effects of vindoline administration on male reproductive function as well as the overall safety of treatment with vindoline are necessary.
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DelloStritto, Daniel Justin. "TRPing up the Balance of Oxidative Stress - Transient Receptor Potential Vanilloid 1’s Role in Diabetic Microvascular Disease." NEOMED Integrated Pharmaceutical Medicine / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ne2mh1469567446.
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Cheng, Wing-tim. "Polyol pathway contributes to hyperglycemia-induced cardiac dysfunction." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41508622.
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Spada, Ana Paula Machado. "Avaliação do estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada /." Botucatu : [s.n.], 2009. http://hdl.handle.net/11449/99250.
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Resumo: Objetivo: avaliar o estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada. Métodos: O diabete foi induzido em ratas Wistar recém-nascidas (grupo diabete moderado) no dia do nascimento (dia 0) por streptozotocin (100 mg/kg, via subcutênea). As ratas do grupo nãodiabético (controle) receberam somente tampão citrato. Na vida adulta, as ratas (diabéticas e controle) foram submetidas ao acasalamento e o dia de diagnóstico positivo de prenhez foi considerado dia 0. A glicemia foi determinada nos dias 0, 7, 14 e 21 de prenhez. No 21º dia de prenhez, as ratas foram anestesiadas e dessangradas para determinação das atividades enzimáticas de superóxido dismutase (SOD), glutationa peroxidase (GSH-Px) e glutationa redutase (GSH-Rd) e das concentrações de grupos tiólicos (SH) e de espécies reativas ao ácido tiobarbitúrico (TBARS). Em seguida, as placentas foram retiradas e processadas para determinação das atividades de SOD e catalase e concentração de TBARS, gluationa reduzida e grupos tiólicos. Resultados: Ratas com diabete induzido no período neonatal (grupo diabético) apresentaram glicemia superior a 120mg/dl no dia 0 de prenhez e foi observada hiperglicemia no 14º dia de prenhez. A análise do estresse oxidativo em hemáceas lavadas mostrou que no grupo diabético houve aumento significativo na atividade da GSH-Px. No tecido placentário a atividade da catalase foi significativamente maior em ratas com diabete moderado. Conclusão: Frente às condições experimentais analisadas, o aumento dos biomarcadores do sistema antioxidante em ratas com diabete de intensidade moderada foram suficientes para conter o estresse oxidativo.Abstract: Objective: To evaluate the oxidative stress in blood sample and placental of female rats that received streptozotocin in the neonatal period. Methods: The diabetes was induced in female offspring (diabetic group) in the day of the birth (day 0) for streptozotocin (100 mg/kg, subcutaneous route). Female control rat (control group) received only citrate buffer. In the adult life, the female rats were submitted to the mating and the day the positive diagnosis, was considered day 0 of pregnancy. The glycemia was measured in the 0, 7, 14 and 21 of pregnancy. At day 21 of pregnancy, the female rats were anesthetized and died by decapitation for collection of the blood for determination of the enzymatic activity of the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and of the concentrations of thiols group and thiobarbituric acid reactive substances (TBARS). Afterwards, placental were removed and processed for determinations of the enzymatic activity of the SOD and catalase and of the concentrations of the TBARS, glutathione reduced (GSH) and thiols group (SH). Results: Diabetic rats presented blood glucose concentration greater than 120 mg/dL in the day 0 of pregnancy and hyperglycemia in 14 º day of pregnancy. The analysis of the oxidative stress in maternal blood sample showed increased in GSH-Px activity. In placental tissue catalase activity of diabetic group is found to be increase in homogenate tissue in diabetic group. Conclusion: The hyperglycemia in diabetic rats increased antioxidant system biomarkers, however, these alterations were enough to control oxidative stress.
Orientador: Débora Cristina Damasceno
Coorientador: Tiago Rodrigues
Mestre
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Macedo, Nathália Cristine Dias. "Avaliação da prática de exercício físico (natação) de intensidade moderada no estresse oxidativo, hormônios sexuais e proliferação pancreática de ratas diabéticas prenhes." Botucatu, 2016. http://hdl.handle.net/11449/137838.
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Orientador: Débora Cristina DamascenoResumo: Objetivo: Avaliar os marcadores de glicemia, proliferação e estresse oxidativo de ratas com diabete moderado submetidas ao exercício físico (natação) de intensidade moderada durante a prenhez. Método: Foram utilizadas ratas da linhagem Wistar. O diabete moderado foi induzido em recém-nascidos (RN) fêmeas no primeiro dia de vida (100 mg de Streptozotocin®/kg de peso corpóreo, via subcutânea). Para compor o grupo não diabético, os RN receberam o veículo em volume e período similares ao grupo diabético. Na fase adulta, todos os animais foram submetidos ao acasalamento e, confirmada a prenhez, foram distribuídos em quatro grupos: não diabético não exercitado, não diabético exercitado, diabético não exercitado e diabético exercitado. As ratas dos grupos submetidos à natação de intensidade moderada durante a prenhez carregaram cargas equivalentes a 4% do peso corpóreo. No 18º dia de prenhez, as ratas foram anestesiadas e mortas para análise do desempenho reprodutivo, marcadores bioquímicos e de estresse oxidativo e análises morfométrica e imunoistoquímica do pâncreas materno. Resultados: A natação alterou o metabolismo glicêmico de forma positiva e melhorou a capacidade de defesa antioxidante em ratas não diabéticas, contribuindo para o bom desempenho reprodutivo materno. Em animais diabéticos, a natação não alterou a função pancreática, aumentou danos musculares, diminuiu a defesa antioxidante, causou estresse oxidativo, mas não causou prejuízo ao desenvolvimento fetal. Conclusão:... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Objective: To evaluate glycemic, proliferation and oxidative stress markers in moderate diabetic rats submitted to moderate intensity swimming during pregnancy. Methods: Wistar rats were used. At birth, female rats were assigned either to control or diabetic group (100 mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated and confirmed the pregnancy, were divided into four groups: nondiabetic non exercised, nondiabetic exercised, diabetic non exercised and diabetic exercised. The exercised groups carried loads equivalent to 4% of body weight. The rats were used for analysis of reproductive performance, oxidative stress biochemical markers and morphometric and immunohistochemical analysis of endocrine pancreas. Results: Swimming altered carbohydrate metabolism positively and improved the antioxidant defense in nondiabetic rats, which contributes to good maternal reproductive performance. In diabetic animals, swimming did not affect pancreatic function, increased muscle damage, decreased antioxidant defense, but did not cause damage to fetal development. Conclusions: Therefore, swimming moderate exercise was beneficial to nondiabetic rats. This same exercise conditions established for healthy animals, however, should not be applied to diabetic rats because it have different responses presented in our study after the implementation of the exercise.
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Assis, Renata Pires de. "Efeito da curcumina e carotenoides em iogurte sobre biomarcadores fisio-metabólicos e de estresse oxidativo em modelos de diabetes mellitus tipo 1 e de obesidade/resistência insulínica /." Araraquara, 2016. http://hdl.handle.net/11449/144510.
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Orientador: Iguatemy Lourenço BrunettiCoorientador: Amanda Martins Baviera
Banaca: Mauro Sola-Penna
Banaca: Luciana Chagas Caperuto
Banaca: Katia Sivieri
Banaca: Ana Angélica Henrique Fernandes
Resumo: As mudanças no estilo de vida e na estrutura dietética da população atual levam a uma ingestão calórica excessiva e ao comportamento sedentário, que em conjunto pode explicar a epidemia de obesidade e diabetes mellitus (DM). O diabetes mellitus é definido como um grupo de doenças metabólicas caracterizado por hiperglicemia, resultante da deficiência na produção e secreção de insulina pelas células beta pancreáticas e/ou resistência à ação da insulina em tecidos-alvo. A manutenção da hiperglicemia por longos períodos é um dos principais fatores envolvidos no estabelecimento do estresse oxidativo, condição esta que participa no desenvolvimento de vários prejuízos do DM, em especial as complicações micro e macrovasculares. Diversos trabalhos demonstram os efeitos de produtos naturais na melhoria da hiperglicemia, estresse oxidativo, status inflamatório e nas complicações do DM. Também tem sido explorado o uso de matrizes alimentares como veículos para ativos naturais, como por exemplo, o iogurte. Neste contexto, utilizamos dois modelos experimentais para avaliar os efeitos dos tratamentos com curcumina, bixina ou licopeno incorporados ao iogurte, isolados ou em associação: i) DM tipo 1 induzido com estreptozotocina (STZ); ii) obesidade/resistência insulínica induzida com dieta high-fat (HF). Experimento I: No modelo de DM induzido com STZ, foram utilizados ratos Wistar machos, normais (N) e diabéticos (D, 40 mg/kg STZ, i.v.), tratados durante 50 dias, distribuídos nos seguintes ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The changes in lifestyle and in dietary structure of the current population lead to an excessive caloric intake and sedentary lifestyle, which can explain the epidemic proportions of obesity and diabetes mellitus (DM). DM is defined as a group of metabolic diseases characterized by hyperglycemia resulting from deficiency in the production and secretion of insulin by pancreatic beta cells and/or resistance to the insulin action in target tissues. The maintenance of hyperglycemia for long periods is a major factor in establishing the oxidative stress, which participates in the development of several impairments of diabetes, especially the microvascular and macrovascular complications. Many studies are demonstrating the effects of natural products on improving the hyperglycemia, oxidative stress, inflammatory status and the DM complications. Food matrices have been also explored as vehicle for natural actives, such as the yoghurt. In this context, we used two experimental models for assessing the effects of the treatments with curcumin, bixin or lycopene incorporated in yoghurt, isolated or in mixtures: i) type 1 DM induced by streptozotocin (STZ); ii) obesity/insulin resistance induced by high-fat (HF) diet. Experiment I: In DM model induced by STZ, male Wistar rats, normal (N) and diabetic (D, 40 mg/kg STZ, i.v.) animals, they were treated for 50 days, according to the following groups: NYOG and DYOG, treated with yoghurt; DINS, treated with insulin (4 U/day); DC, treated with 90 mg/kg curcumin; DB, treated with 5.5 mg/kg bixin; DCB, treated with 90 mg/kg curcumin and 5.5 mg/kg bixin; DL, treated with 45 mg/kg lycopene; DCL, treated with 90 mg/kg curcumin and 45 mg/kg lycopene. All natural compounds were administered with yoghurt. The following parameters were analyzed: i) physiological parameters: body weight, food... (Complete abstract click electronic access below)
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