Abstract
Objective: The present study assessed the hepatotoxicity and nephrotoxicity associated with oxidative stress induced by chronic exposure to a very low environmentally relevant dose of hexavalent chromium along with the ameliorative potential of selenium and Vitamin E in male rats.
 Methods: Twenty-four male albino rats were divided into four groups. Animals of control group received only distilled water. The treated group received solution of potassium dichromate (K2Cr2O7) at a dose of 1 mg/kg b.w./day. The third group received sodium selenate (0.25 mg/kg bw) plus Vitamin E (100 mg/kg bw). The supplemented group received sodium selenate plus Vitamin E along with K2Cr2O7 solution. The animals were treated for 90 consecutive days.
 Results: There was a significant decrease in body weight gain and an increase in liver and kidney weight along with an increase in serum glucose, cholesterol, urea, and creatinine; a decrease in protein and albumin levels in the rats treated with K2Cr2O7. The activities of serum enzymes, serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, acid phosphatase, and alkaline phosphatase, were also increased in treated animals. The activities of enzymes catalase, superoxide dismutase, GPx and the levels of GSH reduced significantly and level of malondialdehyde increased in K2Cr2O7 treated rats. Liver and kidney tissues exhibited features of toxicity in chromium treated animals. All the effects were reversed in supplemented group.
 Conclusion: Chronic exposure to K2Cr2O7 at a very low environmentally relevant dose caused hepatotoxicity and nephrotoxicity induced by oxidative stress in male albino rats; the effects were ameliorated by supplementation with selenium and Vitamin E in combination.
Highlights
Oral exposure to hexavalent chromium (Cr VI) produces gastrointestinal, haematological, hepatic, renal and neurological defects [1]
Effect on body weight gain and organ weight There was a significant reduction in percentage gain of body weight after chronic exposure to chromium (1 mg/kg body weight/day) for 90 consecutive days
Weight of both liver and kidney was increased significantly in animals exposed to chromium (Group-II) in comparison to control animals (Group-I)
Summary
Oral exposure to hexavalent chromium (Cr VI) produces gastrointestinal, haematological, hepatic, renal and neurological defects [1]. Long-term chronic exposure to chromium causes renal injury and produces renal dysfunction [3]. Most of these reports were based on studies with short time exposure at very high exposure doses. Cr VI and its intermediates are capable of generating reactive oxygen specie (ROS), leading to oxidative stress. It reduces the antioxidant capacity by decreasing the activities of different enzyme systems associated with antioxidant defense mechanisms [5]. Chromium is reported to cause both hepatotoxicity and nephrotoxicity through oxidative stress mediated mechanism in experimental animals [6]
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