Effect of Zinc on Hepatic and Renal Tissues of Chronically Arsenic Exposed Rats: A Biochemical and Histopathological Study.

Abstract

Consumption of arsenic-contaminated drinking water has become major global health concern. One of the major mechanism responsible for the toxicity of arsenicals is the generation of oxidative stress. Zinc, a nutritional antioxidant, plays key role in maintaining various cellular pathways. The present study was aimed at elucidating the effects of zinc supplementation on hepatic and renal tissue damage caused by arsenic exposure to rats. Rats were randomly divided into four experimental groups: control; As administered; Zn supplemented; combined zinc; and arsenic supplemented. Arsenic exposure resulted in significantly elevated accumulation of arsenic in the liver and kidney tissue. In the liver, exposure to arsenic reduced the levels of reduced glutathione (GSH), total glutathione (TG), redox ratio, and the activity of superoxide dismutase (SOD), whereas lipid peroxidation (LPO), inflammation markers, and nitric oxide (NO) levels were elevated with no significant change in catalase (CAT) activity. Arsenic exposure also enhanced the serum levels of liver functional indices and histological abnormalities in liver sections. In the kidney, a significant increase in NO levels and decrease in SOD activity was observed, with no significant changes in the rest of the parameters. The administration of zinc- to arsenic-intoxicated animals significantly improved their hepatic function parameters, arsenic burden, and histological changes which were associated with the restoration of enzymatic and non-enzymatic antioxidant defense system as compared to their intoxicated counterparts. In the kidney also, the NO levels and SOD activity were restored. This data reveals that zinc is effective in ameliorating the toxic effects inflicted by chronic arsenic toxicity.