Short term effects of crude oil, vanadium and nickel intoxication on rats liver antioxidant defence system

Abstract

Lipid peroxidation (LPO) and alterations in cellular systems protecting against oxidative damage were determined in the liver of male albino rats, 4 weeks after intraperitoneal (i.p) injection of 0.5 ml/kg bw of crude oil and/or oral consumption of 150 mg V /L or 180 mg Ni /L. After subjecting the rats to crude oil or vanadium or nickel, LPO level and serum alanine-(ALT) and aspartate-(AST) transaminases activities were raised (p<0.01) but the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activities were decreased (p<0.01) signifi cantly. Signifi cant increase (p<0.001) was observed in the glutathione content in nickel-treated rats whereas glutathione content in crude oil or vanadium-treated rats was signifi cantly (p<0.001) inhibited. Glutathione-S-transferase (GST) activity was found to be increased (p<0.001) after crude oil exposure while vanadium or nickel exposure decreased (p<0.001) the GST activity. In conclusion, crude oil, vanadium and nickel treatments caused profound cell damage as indicated by increased LPO in liver and leakage of intracellular enzymes, ALT and AST to the blood; concomitant exposure to crude oil and vanadium exacerbated this effect in a synergistic manner. Stimulation of GSH synthesis by administration of nickel reduced crude oil induced toxicity. The toxicity induced by simultaneous administration of vanadium, nickel and crude oil is less than single toxicity of these metals and crude oil.