Abstract
In this investigation, hepatorenal antioxidant effects of combined oral administration of ammonium metavanadate (AMV; 0.15 mg V/ml) and nickel sulfate (NS; 0.18 mg Ni/ml) in male albino rats over a 21- day period have been evaluated. After administration of vanadium, lipid peroxidation (LPO) increased significantly (p 0.05) in liver, superoxide dismutase (SOD) and glutathione –S-transferase (GST) activities increased significantly in kidney (p < 0.01) and decreased in liver (p < 0.001) whereas glutathione (GSH) content decreased (p < 0.001) in both organs. The exposure to nickel led to a significant decrease (p < 0.001) in SOD, GST activities in liver and GSH content in kidney and a significant (p < 0.001) increase in the hepatic MDA content and renal SOD activity. When the metals were administered in combination, the elevation of lipid peroxidation did not potentiate. However, the inhibition in hepatic SOD was augmented. In the other hand, the combined metals treatment slightly improved the decreased hepatic GST activity and induced the hepatorenal content of GSH. Signs of toxicity were observed following treatment with vanadium, not nickel nor combined vanadium and nickel. A reduction in cellular enzymatic (SOD) and non-enzymatic (GSH) antioxidants is clearly indicative of oxidative stress. The results of this study indicate that kidney is more vulnerable to the caused by vanadium and/or nickel-induced oxidative stress than liver, the oxidative capacity of nickel is much lower than vanadium as well as that the oxidative capacity of combined vanadium and nickel may be more markedly decreased than at separate exposure. Key words: Oral, vanadium, nickel, antioxidant, hepatorenal, rats.