Hoda E. A. Farid, Medhat M. Abozid*, Kamal E. Mahmoud Department of Biochemistry, Faculty of Agricultural, Minufiya University (EGYPT) *Corresponding author: medh_latef@yahoo.com DOI: 10.7813/2075-4124.2012/4-5/A.2 ABSTRACT The present study was performed to investigate short term effects of vanadium and nickel intoxication on rats liver antioxidant defence system. After 4 weeks of oral treatment of 150 mg vanadium (V) /L or 180 mg nickel (Ni) /L and their combination. At the end of treatment, malondialehyde (MDA) level in liver tissues and serum alanine-(ALT) and aspartate-(AST) aminotransferase activities were increased but the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activities were decreased significantly. Significant decrease was observed in the glutathione (GSH) content in all groups compared with control. Glutathione-S-transferase (GST) activity was showed the same behavior. Joint action analysis of vanadium, nickel and their mixture, depending upon biochemical data measurements showed antagonistic (An) effects in ALT, AST, GST, GSH, SOD and MDA while, additive effect (Ad) was found in CAT. In conclusion, vanadium and nickel treatments caused profound cell damage as indicated by increased MDA in liver and leakage of intracellular enzymes, ALT and AST to the blood, as well as decrease in antioxidant biomarkers. Key words: vanadium, nickel, antioxidant enzymes, malondialdehyde, rat. 1. INTRODUCTION There has been a growing interest for heavy metals, in recent years, studies on impact of trace heavy metals have continued to assume increasing relevance especially in the areas of petroleum chemistry and toxicology [1]. Metals play important roles in a wide variety of biological processes of living systems. Homeostasis of metal ions, maintained through tightly regulated mechanisms of uptake, storage and secretion is therefore critical for life and is maintained within strict limits [2]. Despite the fact that some studies showed its beneficial pharmaceutical effects, vanadium therapeutically exposure and the exposure associated with taking vanadium supplements, especially those which can provide more than 10 mg V/day [3], should be taken into consideration. Long-term intake of even small doses of vanadium could be toxic; no recommended dietary allowance has been clearly established [4]. The main target organ for nickel induced toxicity in animals is the respiratory tract [5]. The toxicity of nickel compounds appears to be related to the solubility of the compound. Several acute animal studies have reported soluble nickel sulfate as being the most toxic and insoluble nickel oxide the least toxic [6]. Vanadium and nickel metals not only are present in residual waters from the oil industry but also can be present as particulate matter in inhaled air [7] and as environmental heavy metals emitted from automotive materials [8]. Both metals are also present as aerosols or in the ashes of thermal power stations operating on oil fuel [9]. The recovery of heavy metals from industrial residues is an important task for environmental and economic reasons [10]. Although toxicity of individual heavy metals has been studied extensively, [11] the toxicological impact of a mixture is relatively less understood. Therefore, studies on mixture of heavy metals are necessary in order to understand their interactions on the living system and to evaluate their risk assessment [12]. Considering the above- stated, the toxic effect of vanadium and nickel in liver of rats after separate and combined exposures was planned to be carried in the present research by using antioxidant indices and marker enzymes of tissue damage (aminotransferases) as biochemical indicators. 2. MATERIALS AND METHODS 2.1. Chemicals Kits for glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were obtained from gamma trade company, Egypt. Ammonium metavanadate (NH