Effect of in mercuric chloride-induced renal accumulation of mercury and nephrotoxicity in rat.

Mercury generates free radicals and subsequently increases oxidative stress, which leads to renal injury. (TT) has good anti-inflammatory and antioxidant properties. Hydroalcoholic extract of different dose of TT was evaluated against mercuric chloride-induced nephrotoxicity. Rats ( = 6) were treated with TT at doses of 100, 200, and 300 mg/kg. Drugs were administered orally for 7 days. Single dose of mercuric chloride (5 mg/kg, intraperitoneal) on the 5 day caused significant elevation of blood urea nitrogen, serum creatinine, malondialdehyde, liver fatty acid binding protein, kidney injury molecule-1, and kidney mercury level and fall in glutathione, superoxide dismutase, glutathione peroxidase, and histopathological changes in disease control as compared to normal control group ( < 0.001). Dose of TT 200 and 300 mg/kg significantly ( < 0.001) prevented the renal injury, and mercury accumulation in kidney tissues significantly decreases in higher dose, i.e., 300 mg/kg as compared to control group. Our result indicates that the treatment of TT exerted significant protection against renal damage induced by mercuric chloride possibly due to its antioxidant and anti-inflammatory properties and by decreasing the renal accumulation of mercury.