The aim of the present study was to elucidate the possible protective role of vitamin E and / or sodium selenite on mercuric chloride-induced oxidative stress and histopathological changes in the lung tissue of the rats. Adult male albino Wistar rats were exposed to mercuric chloride (1.0 mg/kg day) for four weeks. Treatment with mercuric chloride led to oxidative stress by enhancing MDA level and also decreasing superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S transferaz (GST) activities. However, mercuric chloride exposure resulted in histopathological changes in the lung tissue in the rats. MDA level and SOD, CAT GPx and GST activities and histopathological changes modulated in concomitantly supplementation of vitamin E (100 mg/kg day) and /or sodium selenite (0.25 mg/kg day) to mercuric chloride-treated groups.
Mercuric chloride; Sodium selenite; Vitamin E; Lung toxicity; Oxidative stress; Histopathology
), fibrosis (
), infiltration of inflammatory cells (
), ×200. (D-E respectively) Lung section of vitamin E + mercuric chloride - and sodium selenite + mercuric chloride -treated rats showing infiltration of inflammatory cells (
), hemorrhage (
), interalveolar septa thickening (