Beneficial Effect Administration of Vitamin C in Amelioration of Lead Hepatotoxicity
Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipid. Oxidative stress with subsequent lipid peroxidation has been postulated as one mechanism for lead toxicity. The protective action of vitamins C against lead affects lipid hydroperoxide level and liver functions in male rats has been studied. Experiments were performed on male waster rats with body weights of 120-160 g. Male wistar rats were exposed to 3 g/l lead acetate in drinking water for 5 weeks and treated thereafter with vitamin C (500 mg/kg, orally) for 28 days. One day after the feeding was over, venous blood samples, under chloroform anesthesia, were collected. The animals were killed by exsanguinations and the liver was excise for determination the metal content and histopathological changes. Similarly, the tissue lipid (lipid peroxidation) and the enzyme fraction (superoxide dismutase (SOD), catalase (CAT), alkaline phosphatase (ALP), acid phosphatase (ACP) and glutathione (GSH) were also measured in the liver. Metal content in blood and liver was determined by means of atomic absorption spectrophotometry. Administration of lead acetate (3 g/l) in drinking water for 5 weeks induced a significant increase in the levels of hepatic ALP, ACP and lipid peroxidation. Lead acetate exposure also produced detrimental effects on the redox status of the liver indicated by a significant decline in the levels of liver antioxidants such SOD, CAT and GSH. Further, there was a significant increase in the levels of lead in blood and liver of animals exposed to lead. However, oral administration of vitamin C at dose level of 500 mg/kg body weight reduced the alterations in the previous parameters. Histological examination of the liver also revealed pathophysiological changes in lead acetate-exposed group and treatment with vitamin C improved liver histology. The result of this study strongly indicate that vitamin C has got a potent antioxidant action against lead acetate induced hepatic damage in rats.
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