706 resultados para peroxidation


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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Medicina Veterinária - FCAV

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Introduction: skeletal muscles are dynamic tissue that can change their phenotypic characteristics providing a better functional adaptation to different stimuli. L-thyroxine is a hormone produced by the thyroid gland and has been used as an experimental model for stimulation of oxidative stress in skeletal muscle. Coenzyme Q10 (CoQ10) is a fat-soluble provitamin endogenously synthesized and found naturally in foods such red meat, fish, cereals, broccoli and spinach. It has antioxidant properties and potential in the treatment of degenerative and neuromuscular diseases. Objective: to evaluate the protective effect of CoQ10 in the soleus muscle of rats against the oxidative damage caused by L-thyroxine. Methods: the rats were divided in four groups of six animals each: Group 1 (control); Group 2 (coenzyme Q10); Group 3 (L-thyroxine), and Group 4 coenzyme Q10 and L-thyroxine). After euthanasia, blood was collected and serum activity of the enzymes creatine kinase (CK) and aspartate aminotransferase (AST) was analyzed. In the soleus muscle homogenates the factors related to oxidative stress were assessed. Results: CoQ10 protected the soleus muscle against the damage caused by L-thyroxine and favored the maintenance of the antioxidant enzymes glutathione reductase and glutathione peroxidase, the concentration of decreased and oxidized glutathione, and prevented lipid peroxidation. Conclusion: the results indicate that CoQ10 protects rat soleus muscle from oxidative damage caused by L-thyroxine.

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Background: The liver is an important organ for its ability to transform xenobiotics, making the liver tissue a prime target for toxic substances. The carotenoid bixin present in annatto is an antioxidant that can protect cells and tissues against the deleterious effects of free radicals. In this study, we evaluated the protective effect of bixin on liver damage induced by carbon tetrachloride (CCl4) in rats.Results: The animals were divided into four groups with six rats in each group. CCl4 (0.125 mL kg(-1) body wt.) was injected intraperitoneally, and bixin (5.0 mg kg(-1) body wt.) was given by gavage 7 days before the CCl4 injection. Bixin prevented the liver damage caused by CCl4, as noted by the significant decrease in serum aminotransferases release. Bixin protected the liver against the oxidizing effects of CCl4 by preventing a decrease in glutathione reductase activity and the levels of reduced glutathione and NADPH. The peroxidation of membrane lipids and histopathological damage of the liver was significantly prevented by bixin treatment.Conclusion: Therefore, we can conclude that the protective effect of bixin against hepatotoxicity induced by CCl4 is related to the antioxidant activity of the compound.

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Inhaled anaesthetics have been studied regarding their genotoxic and mutagenic potential in vivo. Propofol differs from volatile anaesthetics because it does not show mutagenic effects and it has been reported to be an antioxidant. However, there are no studies with propofol and genotoxicity in vivo. The study aimed to evaluate the hypothesis that propofol is not genotoxic and it inhibits lipid peroxidation [malondialdehyde (MDA)] in patients undergoing propofol anaesthesia. ASA physical status I patients scheduled for elective surgery, lasting at least 90 min, were enrolled in this study. Initially, the estimated plasma concentration of propofol was targeted at 4 microg ml(-1) and then maintained at 2-4 microg ml(-1) until the end of surgery. Haemodynamic data were determined at baseline (before premedication) and in conjunction with target-controlled infusion of propofol: after tracheal intubation, 30, 60 and 90 min after anaesthesia induction and at the end of the surgery. Venous blood samples were collected at baseline, after tracheal intubation, at the end of the surgery and on the postoperative first day for evaluating DNA damage in white blood cells (WBCs), by comet assay, and MDA levels. Haemodynamic data did not differ among times. No statistically significant differences were observed for the levels of DNA damage in WBCs, nor in plasma MDA, among the four times. Propofol does not induce DNA damage in WBCs and does not alter MDA in plasma of patients.

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