Protective role of Ellagic acid in modulating Iron induced Nephrotoxicity in rats

Iron (Fe) is an environmental and industrial pollutant that affects various organs in human and animals. A body of evidence implicates that the free radical generation with subsequent oxidative stressis involved in the mechanism of Fe toxicity. Since the kidney is critical target of Fe toxicity we carried out this study to investigate the effect of Ellagic acid (EA), a polyphenolic compound on renal injury induced by Fe. In this study, Fe (30mg/kg body weight was administered intraperitoneally for 10 days to induce toxicity. EA was administered orally (15, 30 and 60mg/kg body weight) for 10days along with Fe. Fe induced renal damage was indicated by the increased activities of serum urea and creatinine along with reduced renal clearance. A significant increase in lipid peroxidation markers (TBARS and lipid hydroperoxide) was observed in kidney of Fe treated rats. Rats subjected to Fe toxicity also showed a decline in the levels of reduced glutathione (GSH), vitamin C and vitamin E together with significantly decreased levels of enzymic antioxidants superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX). Administration of EA at 60 mg/kg body weight attenuated the Fe induced nephrotoxicity indicated by significantly decreased levels of serum urea and creatinine with normalization of creatinine clearance. On administration of EA, the depleted renal antioxidant defense system (enzymatic and non enzymatic antioxidants) was significantly increased in Fe treated rats. The biochemical observations were supplemented by histopathological examination of kidney section. Our results suggest that supplementation of EA might be helpful to alleviate the Fe induced oxidative injury in kidney.