We studied the effect of zinc treatment on nickel sulphate-induced hepatotoxicity in male albino rats. Liver dysfunction parameters represented by aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), blood glucose, serum total protein and serum albumin were estimated. Liver glutathione level, catalase and GPx activities were also determined in liver as indicators of oxidative damage. Exposure of rats to nickel caused a significant a decrease in body weight and an increase in liver weight compared to the controls. Nickel treatment was also led to high glucose concentration and produced hepatotoxicity characterized by increasing GPT, GOT and alkaline phosphatase activities. Meanwhile nickel administration resulted in low serum total protein and serum albumin. In addition liver glutathione level, catalase and GSH-Px activities were diminished due to high lipid peroxidation. Meanwhile the administration of zinc with nickel resulted in a remarkable improvement of the previous parameters comparison with rats treated with nickel alone. Liver histological studies have confirmed the changes observed in biochemical parameters and proved the beneficial role of zinc. In conclusion, nickel sulphate led to liver dysfunction and hepatic lipid peroxidation in animals, but simultaneous treatment with zinc offers a relative protection against nickel induced hepatotoxicity and lipid peroxidation probably due to its antioxidant proprieties.
Ion channels cell biochemistry biophysics calcium signaling cellular function cellular physiology metabolism apoptosis lipid peroxidation nitric oxide synthase ageing antioxidants neuropathy
Primary Language | English |
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Journal Section | Original Articles |
Authors | |
Publication Date | August 14, 2013 |
Published in Issue | Year 2011 Volume: 3 Issue: 2 |