Publications (137) View all
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Article: Water-immersion restraint stress disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats.
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ABSTRACT: We examined whether water-immersion restraint stress (WIRS) disrupts nonenzymatic antioxidant defense systems through ascorbic acid depletion in the adrenal gland of rats. Rats were exposed to WIRS for 0.5, 1.5, 3 or 6 h. WIRS increased serum adrenocorticotropic hormone, corticosterone and glucose concentrations and adrenal corticosterone content at each time point. WIRS increased adrenal lipid peroxide content at 3 and 6 h, and the increase was twofold higher than the unstressed level at 6 h. WIRS decreased adrenal ascorbic acid content at each time point, and the decrease reached one-third of the unstressed level at 6 h. WIRS increased adrenal reduced glutathione content at 0.5 and 6 h but reduced that content to half of the unstressed level at 6 h. WIRS increased adrenal α-tocopherol content at 1.5 h but returned that content to the unstressed level thereafter. When rats with 6 h of WIRS was orally preadministered with l-ascorbic acid (250 mg/kg), WIRS-induced changes in adrenal lipid peroxide, ascorbic acid and reduced glutathione contents were attenuated without any change in stress response. These results indicate that WIRS disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats. Copyright © 2012 John Wiley & Sons, Ltd.Cell Biochemistry and Function 09/2012; · 1.77 Impact Factor -
Article: Disruption of non-enzymatic antioxidant defense systems in the brain of rats with water-immersion restraint stress.
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ABSTRACT: We examined whether non-enzymatic antioxidant defense systems are disrupted in the brain of rats with water-immersion restraint stress. When rats were exposed to water-immersion restraint stress for 1.5, 3 or 6 h, the brain had decreased ascorbic acid and reduced glutathione contents and increased lipid peroxide and nitric oxide metabolites contents at 3 h and showed further changes in these components with a reduction of vitamin E content at 6 h. Increased serum levels of stress markers were found at 1.5, 3 or 6 h of WIRS. Oral pre-administration of L-ascorbic acid (1.5 mmol/kg) or vitamin E (0.5 mmol/kg) to rats with 6 h of water-immersion restraint stress attenuated the increases in lipid peroxide and nitric oxide metabolites contents and the decrease in vitamin E content in the brain. Pre-administered L-ascorbic acid attenuated the decreases in brain ascorbic acid and reduced glutathione contents at 6 h of water-immersion restraint stress, while pre-administered vitamin E enhanced the decreases in those contents. Pre-administered L-ascorbic acid or vitamin E did not affect the increased serum levels of stress markers in rats with 6 h of water-immersion restraint stress. These results indicate that water-immersion restraint stress causes disruption of non-enzymatic antioxidant defense systems through enhanced lipid peroxidation and nitric oxide generation in the brain of rats with water-immersion restraint stress.Journal of Clinical Biochemistry and Nutrition 09/2012; 51(2):136-42. · 1.98 Impact Factor -
Article: Metabolic Syndrome, Its Pathophysiology and the Role of Melatonin.
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ABSTRACT: Metabolic syndrome is characterised by symptoms of obesity, insulin resistance, hypertension, dyslipidemia and diabetes mellitus. The pathophysiological mechanisms involved in MetS are complex and involve dysregulation of many biochemical and physiological regulatory mechanisms of the body. Elevated levels of low density lipoproteins like VLDL, and LDL with reduction of HDL seen in patients with MetS contribute to atherogenic dyslipedemia. Melatonin has been suggested to be effective in improving MetS through its anti-hyperlipidemic action .Melatonin reduced both adiposity, and body weight in experimental animal studies and also attenuated weight gain and obesity induced metabolic alterations and this effect of melatonin is attributed to its anti-oxidative effects. Melatonin administration has been shown to inhibit insulin release by acting through both MT1and MT2 melatonin receptors present in pancreatic β-cells. Melatonin also increased insulin sensitivity and glucose tolerance in animals fed with either high fat or high sucrose diet .Melatonin exerts most of its beneficial actions by acting through MT1 and MT2 melatonin receptors present in various tissues of the body and some of the metabolic actions of melatonin have been blocked by melatonin antagonist like luzindole. Ramelteon,the newly available melatonin agonist will have also more promising role in the control of MetS. Numbers of patents are available with regard to treatment of MetS. Drug related to antidepressant fluoxetine is used for treatment of MetS (US patent No. 2008001400450). Antioxidants like S adenosylmethionine, vitamin-E, and vitamin C have been found beneficial in treating Mets (US patent No. 8063024). Melatonin being a powerful antioxidant will have a promising role in treating patients with metabolic syndrome.Recent Patents on Endocrine Metabolic & Immune Drug Discovery 08/2012; -
Article: Protective Effect of Brazilian Propolis Against Hepatic Oxidative Damage in Rats with Water-immersion Restraint Stress.
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ABSTRACT: In the present study we examined the protective effect of Brazilian propolis against hepatic oxidative damage in rats with water-immersion restraint stress (WIRS) in comparison with that of vitamin E (VE). Fasted rats orally received Brazilian green propolis ethanol extract (BPEE; 10, 50 or 100 mg/kg), VE (250 mg/kg) or vehicle at 30 min before the onset of WIRS. Exposure of vehicle-treated rats to 6 h of WIRS caused liver cell damage, judging from the levels of serum alanine aminotransferase and aspartate aminotransferease, increased hepatic lipid peroxide, NO(x) contents and myeloperoxidase activity, and decreased hepatic non-protein SH, ascorbic acid contents and superoxide dismutase activity. Preadministration of BPEE (50 or 100 mg/kg) or VE to the stressed rats protected against the hepatic damage and attenuated the increased hepatic lipid peroxide and NO(x) contents and myeloperoxidase activity and the decreased hepatic non-protein SH and ascorbic acid contents and superoxide dismutase activity. These protective effects of BPEE (50 mg/kg) were greater than those of BPEE (100 mg/kg) and were almost equal to those of VE. These results indicate that BPEE protects against hepatic oxidative damage in rats exposed to WIRS possibly through its antioxidant and antiinflammatory properties such as VE. Copyright © 2012 John Wiley & Sons, Ltd.Phytotherapy Research 02/2012; 26(10):1482-9. · 2.09 Impact Factor -
Article: A single exposure of rats to water-immersion restraint stress induces oxidative stress more severely in the thymus than in the spleen.
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ABSTRACT: We examined whether a single exposure of rats to water-immersion restraint stress (WIRS) induces oxidative stress in the thymus and spleen. Vitamin E, ascorbic acid, reduced glutathione (GSH), and lipid peroxide (LPO) were assayed in the thymus and spleen of rats with and without 6 hours of WIRS. In unstressed rats, vitamin E, ascorbic acid, GSH, and LPO levels were higher in the thymus than in the spleen. Thymic ascorbic acid level was lower in stressed rats than in unstressed rats. Splenic ascorbic acid level was similar in both groups. Thymic and splenic GSH levels were lower in stressed rats than in unstressed rats but the reduced amount of GSH was lower in the spleen than in the thymus. Thymic vitamin E level was lower in stressed than in unstressed rats. Splenic vitamin E level was higher in stressed rats than in unstressed rats. Thymic and splenic LPO levels were higher in stressed rats than in unstressed rats but the increased amount of LPO was higher in the thymus than in the spleen. It is indicated that a single expose of rats to WIRS induces oxidative stress more severely in the thymus than in the spleen.Redox report: communications in free radical research 01/2012; 17(5):200-5. · 1.51 Impact Factor
