Protective role of zinc in ameliorating arsenic-induced oxidative stress and histological changes in rat liver.

The aim of present work was to gain insight into the role of dietary zinc in ameliorating the adverse effects caused by arsenic on rat liver. Male Wistar rats received arsenic alone in the form of sodium arsenite in drinking water at a dose level of 100 ppm, zinc alone in the form of zinc sulfate in drinking water at a dose level of 227 mg/L, or arsenic + zinc treatments in the combined group for a total duration of 3 months. Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment. Furthermore, arsenic treatment resulted in a significant decrease in hepatic zinc levels. Histological studies showed well-differentiated signs of focal hepatitis, lobular inflammation, prominent hepatocyte degeneration, and severe periportal necrosis. Administration of zinc to arsenic-treated rats significantly decreased the level of LPO but increased the level of GSH compared with arsenic-treated rats. Further, the zinc level and activities of SOD, GPx, GR, and CAT were found to be significantly increased following zinc treatment. The administration of zinc to arsenic-treated rats caused signs of improvement in liver histoarchitecture, but a few focal areas of degeneration and necrosis were still occasionally seen. In conclusion, the results of this study suggest that zinc can be beneficial against arsenic-induced hepatotoxicity in rats.