V Valls — Page 2 | PubMed Health

Nutritional obesity induced by the ingestion of hyperlipidic diet implies a high consume of lipids, which might be involved in oxygen metabolism. Double bound, in the fatty-acid molecules are a vulnerable point to undergo oxidation reactions-generating lipid peroxidation, that are potentially toxic and can produce serious cell injury (alteration in cell permeability and prostaglandins...). To prevent this oxidative injury the aerobic organisms have intracellular mechanisms of defense, the antioxidant systems, that may be classified as enzymatic and nonenzymatic. Vitamin C belongs to the second group and acts as scavenger of free radicals and other species. The purpose of this study was to evaluate the oxygen metabolism in isolated hepatocytes of rats which obesity has been reached by the ingestion of an hyperenergetic olive-oil rich controlled liquid diet and evaluate the effect of ascorbic acid. Cellular oxidative injury in isolated hepatocytes was induced through a lipid peroxidative and cytotoxic molecule tert-butyl-hydroperoxide (t-BOOH). Results show higher levels of lactate dehydrogenase (LDH) leakage and malondialdehyde (MDA) production in obese rats as compared with controls. Otherwise, when these groups are supplemented with ascorbic acid these changes decrease significantly. ATP levels decrease in hepatocytes of obese rats incubated in the presence of 1 mM tert-butylhydroperoxide. While it is maintained in ascorbic acid supplemented animals. GSH values were lower in hepatocytes from obese and control rats, incubated with tert-butyl-hydroperoxide. Supplementation with ascorbic acid also maintained GSH levels thus indicating that ascorbic acid is acting as an efficient antioxidant.

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