The present study investigated the hepatoprotective role of
zinc in attenuating the toxicity induced by
chlorpyrifos in rat liver. Male Sprague-Dawley (SD) rats received either oral
chlorpyrifos (13.5mg/kg
body weight),
zinc alone (227mg/l in
drinking water) or combined
chlorpyrifos plus
zinc treatment for a total duration of 8 weeks. The effects of these treatments were studied on various parameters in rat liver, including lipid peroxidation,
antioxidant enzymes, levels of
metallothionein (MT) and hepatic histoarchitecture.
Chlorpyrifos treatment resulted in a significant increase in hepatic lipid peroxidation and activities of
superoxide dismutase (SOD),
glutathione peroxidase (G-Px) and
glutathione reductase (GR). On the contrary,
chlorpyrifos intoxication caused a significant inhibition in the levels of
reduced glutathione (GSH),
catalase (CAT) and
glutathione-S-transferase (GST) activities. However,
zinc treatment to
chlorpyrifos-intoxicated animals normalized the otherwise raised levels of lipid peroxidation to within normal limits. Moreover,
zinc treatment to these animals resulted in an elevation in the levels of GSH,
catalase and GST, as well as a significant decrease in the levels of SOD. Levels of MT were also found to be depressed in
chlorpyrifos-treated animals, but tended to increase following co-administration of
zinc. Additionally,
chlorpyrifos-treated animals demonstrated increased vacuolization,
necrosis and ballooning of the hepatocytes and dilatation of sinusoids as well as increase in the number of binucleated cells. However,
zinc administration to
chlorpyrifos-treated animals resulted in overall improvement in the hepatic histoarchitecture, emphasizing the protective potential of
zinc. Hence, the present study suggests the protective potential of
zinc in alleviating the hepatic toxicity induced by
chlorpyrifos.