الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Vanadium is a trace element distributed extensively in nature and used increasingly in various heavy industries. The liver is considered the primary site of vanadium toxicity. The present study was conducted to investigate the in vitro and in vivo hepatotoxicity of ammonium metavanadate (AMY) and the role of GSH modulation on its hepatotoxicity. The in vitro cytotoxicity and oxidative stress induced by ammonium metavanadate as well as the role of glutathione modulation and free radicals scavengers were investigated on isolated rat hepatocytes. In vitro study, Hepatocytes were isolated by collagenase perfusion technique, the hepatocytes incubated with different concentrations of AMY in a time-course experiment, also hepatocytes pretreated with GSH precursors and depleting agents. in vivo study, live rats were injected with AMY and pretreated with GSH precursors and depleting agents. Our results suggest that AMY cytotoxicity is concentration and time dependent as well as, the GSH depletion plays an important role in enhancing hepatotoxic potential of vanadium. However, GSH boosting, antioxidant enzymes, free radical scavengers and iron chelators markedly protected the cells from AMY cytotoxicity.