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Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.
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Pericyte loss is an early feature of diabetic retinopathy and represents a key step in the progression of this disease. This study aimed to evaluate the effect of dehydroepiandro-sterone (DHEA) on glucose toxicity in retinal capillary pericytes. Bovine retinal pericytes (BRP) were cultured in a high glucose concentration, with or without DHEA. After 4 days of incubation the number of BRP was significantly reduced by the high glucose concentration. The addition of DHEA to the medium reversed the adverse effect of high glucose: BRP proliferation partially recovered in the presence of 10 nmol/l DHEA, and completely recovered in the presence of DHEA at concentrations equal to or greater than 100 nmol/l. At physiological glucose concentrations, DHEA had no effect on BRP growth. Data show that DHEA, at concentrations similar to those found in human plasma, protects BRP against glucose toxicity. This effect seems specific for DHEA, since its metabolites, 5-en-androstene-3 beta, 17 beta-diol, dihydrotestosterone and estradiol did not alter BRP growth in normal or high glucose media. Various pieces of evidence link the antioxidant properties of DHEA to its protective effect on glucose-induced toxicity in BRP.