Effects of benfotiamine and coenzyme Q10 on kidney damage induced gentamicin

2. ABSTRACT Effects of Benfotiamine and Coenzyme Q10 on Kidney Damage Induced Gentamicin Gentamicin is a type of aminoglycoside frequently used in daily clinical practices at treatment of gram negative infections. Coenzyme Q10 (CoQ10) is an endogenous antioxidant and has a protective effect against free radicals. Benfothiamine is a fat soluble type of thiamine vitamin. Our study aims at identifying protective effects of CoenzymeQ10 and benfothiamine against nephrotoxicity induced by gentamicin. 35 Wistar albino rats were used in our study. The rats were divided into five groups. The first group was the control group and the second group was the sham group. In the third group, each rat was administered 80mg/kg/day gentamicin intraperitoneally. In the fourth group, each rat was administered 80mg/kg/day gentamicin intraperitoneally and 10mg/kg/day CoQ10 intraperitoneally. In the fifth group, each rat was administered 80mg/kg/day gentamicin intraperitoneally and 100 mg/kg/day Benfothiamine by oral gavage. After gentamicin, CoQ10 and BFT was administered for eight days, blood samples were taken and renal tissues were extracted after euthanasia. KIM-1, TNFα, glutathione, malondialdehyde, BUN, creatinine were analyzed from blood samples. Tunel dye was rendered and histopathologic observations were evaluated. Serum creatinine, urea, KIM-1 and MDA levels significantly increased in the group administered with gentamicin compared to the control group (P<0.001, P<0.001, P<0.005, P<0.0001, respectively). Although creatinine and KIM-1 levels decreased in the rats administered with gentamicin and coenzymeQ10, this was not statistically significant but serum MDA levels decreased significantly (P<0,001). While serum creatinine, urea, KIM-1, TNFα and MDA levels statistically significantly decreased in the rats administered with gentamicin and benfothiamine (P<0.001, P<0.05, P<0.001, P<0.0001, P<0.0001, respectively), total and reduced glutathione values increased (P<0.0001). Considering on histopathologic terms, a very distinctive necrosis was observed in the tubules in the cortex in the renal tissue in the group administered only with gentamicin. The necrosis highly decreased in the tubules in the cortex at the group administered with gentamicin and benfothiamine. While the necrosis in the cortical tubules in the renal tissues of the subjects administered with gentamicin and CoQ decreased compared to the group administered only with gentamicin, it maintained its distinctiveness compared to the benfothiamine group. In conclusion, this study indicates that benfothiamine and coenzyme Q10 provide protection against gentamicin induced nephrotoxicity and provide it by probably reducing lipid peroxidation induced by gentamicin and exhibiting a protective effect against oxidative damage. Benfothiamine has been demonstrated both biochemically and histopathologically in this study to provide better protection against gentamicin induced nephrotoxicity compared to coenzyme Q10. Especially administering benfothiamine additionally in clinical use of gentamicin as an antibacterial can prove to be an alternative to prevent nephrotoxic side effects. Key Words: Gentamicin, Nephrotoxicity, Oxidative Stress, CoenzymQ10, Benfotiamine