Vitamin E and Selenium Attenuate Hepatotoxicity, Nephrotoxicity and Oxidative Stress Induced by Rifampicin in Rabbits

Rifampicin (RIF) is a first-line anti-tuberculosis drug, besides beneficial effects, it triggers hepatic and renal toxicities. Drug toxicity is assumed to be associated with increased cellular oxidative stress. In the present study, the protective effect of vitamin E (a-tocopherol) and selenium (Se) on hepatic function biomarkers and alteration in renal function against rifampicin-induced toxicity was assessed. Rabbits were selected and placed into six groups (n=6). For 14 days experiment, RIF (100 mg/kg/day) was given to induce hepatorenal toxicity in all animals except normal control. Silymarin (200 mg/kg) was given as standard protective drug. Three groups received Vit. E (50 mg/kg), Se (1 mg/kg) and combination of both, respectively. Blood samples were collected to check hepatic function (ALT, AST, ALP), renal function (creatinine, urea), oxidative stress biomarkers (TOS, TAC, MDA, catalase), and liver and kidney tissue samples for histopathological analysis. Vit. E and Se exhibited significant (P<0.05) protective effect by ameliorating serum levels of ALT, AST, ALP, urea, creatinine against rifampicin induced liver and kidney injury. The protective effect is also evidenced by hepatorenal histopathological analysis. Moreover, elevated oxidative stress accompanied by rifampicin exposure was significantly restored as Vit. E and Se use elevated the serum levels of catalase and TAC, and reduced MDA and TOS. However, Vit. E and Se in combination exhibit a more significant protective effect than alone. Vit. E and Se have therapeutic application in rifampicin associated hepatorenal toxicity presumably through antioxidant properties. (C) 2019 PVJ. All rights reserved