Vitamin-E supplementation ameliorates chromium-and/or nickel induced oxidative stress in vivo

The present study was designed to investigate the in vivo effects of nickel chloride [NiCl2,; 8, and 16 mg/kg body weight (b wt)] and/or Potassium dichromate (K2Cr2O7; 5 and 10 mg/kg b wt) in the liver of adult mice. The beneficial effects of vitamin E (2 mg/kg) along with their combination were also studied. The antioxidative indices including oxidative lipid peroxidation (LPO) and antioxidative enzymes such as glutathione (GSH), total sulfhydryl (-SH) groups, total ascorbic acid (TAA), superoxide dismutase (SOD) and catalase (CAT) were evaluated in the hepatic tissue using well established techniques. Nickel and/or chromium treatments to mice revealed a significant decline in the levels of these antioxidant parameters as compared to control. Concomitantly a significant increase in lipid peroxidation was obtained. These data indicated that the treatment induced oxidative stress in the hepatic tissue of treated mice, which was more pronounced by combination of metal salts. But Supplementation of vitamin E with NiCl2 + K2Cr2O7 to mice exerted no significant alterations in the liver antioxidant system as compared to control, thus indicating its ameliorative role. These findings suggest that vitamin E prevents LPO and protects the antioxidant system in the mouse liver.