Abstract

The present study has been designed to investigate the possible attenuative role of hesperetin (Hp), a citrus flavonone on cadmium (Cd) induced nephrotoxicity in rat using biochemical and histopathological approaches. Administration of Cd subcutaneously at a dose of 3 mg/kg b.w for 21 days significantly induced the renal damage, which was evident from the increased levels of serum urea, uric acid and creatinine with a significant decrease in creatinine clearance. Cd significantly decreased the levels of urea, uric acid and creatinine in urine. The levels of lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and protein carbonyl content (PCC) also significantly increased while the activities of vitamin C, vitamin E, reduced glutathione (GSH), total sulphydryl group (TSH) and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) significantly decreased in the kidney of Cd intoxicated rats. Hp administrated orally along with Cd for 21 days, significantly revert the status of renal markers, urine markers, lipid peroxidation markers and antioxidant defence system of the kidney tissue to near normal level in a dose dependent manner. Hp at a dose of 40 mg/kg b.w exhibited significant ( P < 0.05) nephroprotection when compared with the other two doses. Histological studies on the ultrastructural changes of kidney supported the attenuative role of Hp. Thus, the results suggest that Hp acts as a potent nephroprotective agent against Cd induced nephrotoxicity in rats.

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