Methylmercury Chloride Coaxed Oxidative Stress in Rats

The present experiment was designed to access the effects of Methylmercury chloride ( MeHgCl) on antioxidant status, protein concentration, lipid peroxidation and hydroperoxidation in brain parts, spinal cord, lung, heart and pancreas of rats. Twenty male Wistar rats (3 months old) were divided in saline controls (C) and MeHgCl-treated group (MMC). Treated rats were intoxicated with MMC at a dose of 2 mg/kg body weight orally by gavage once a day for 14 consecutive days, for the next 14 days, they were kept intoxicated. Control animals received a corresponding volume of isotonic saline. Health, total feed intake and body weights of rats were monitored daily throughout the study. Both the groups were sacrificed on 29 th day. Study revealed an increase in Lipid peroxide (LPO) and Lipid hydroperoxide (LHPO) levels after MeHgCl administration. The levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), total sulfhydryl (TSH) and Protein were significantly declined in all the tissues of MMC treated group as compared to controls. In summary, depletion of antioxidant enzymes in tissues increases MeHgCl accumulation and enhances MeHg-induced oxidative stress, especially LPO and LHPO which plays an important role in tissue degeneration process during MeHgCl intoxication. Results support the hypothesis that depletion of antioxidant enzymes is a primary mechanism of organic mercury toxicity. The present experiment was designed to access the effects of Methylmercury chloride ( MeHgCl) on antioxidant status, protein concentration, lipid peroxidation and hydroperoxidation in brain parts, spinal cord, lung, heart and pancreas of rats. Twenty male Wistar rats (3 months old) were divided in saline controls (C) and MeHgCl-treated group (MMC). Treated rats were intoxicated with MMC at a dose of 2 mg/kg body weight orally by gavage once a day for 14 consecutive days, for the next 14 days, they were kept intoxicated. Control animals received a corresponding volume of isotonic saline. Health, total feed intake and body weights of rats were monitored daily throughout the study. Both the groups were sacrificed on 29 th day. Study revealed an increase in Lipid peroxide (LPO) and Lipid hydroperoxide (LHPO) levels after MeHgCl administration. The levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), total sulfhydryl (TSH) and Protein were significantly declined in all the tissues of MMC treated group as compared to controls. In summary, depletion of antioxidant enzymes in tissues increases MeHgCl accumulation and enhances MeHg-induced oxidative stress, especially LPO and LHPO which plays an important role in tissue degeneration process during MeHgCl intoxication. Results support the hypothesis that depletion of antioxidant enzymes is a primary mechanism of organic mercury toxicity.