Role of antioxidant mechanism of L- arginine in gentamicine-induced nephropathy in rats

Nitric oxide synthases (EC 1.14.13.39) (NOSs) are a family of enzymes catalyzing the production of nitric oxide (NO) from L-arginine. In this study ;the benefical effects of L-arginine will be studied in gentamicin (GM) induced nephrotoxicity can be compared to (N-omega-L-arginine methyl ester, a non-selective NOS inhibitör (L- NAME). Several studies have suggested that alterations of the L-arginine (L-Arg) nitric oxide (NO) pathway may be involved in the pathogenesis of gentamicine -induced kidney damage. We aim to study in vivo activation of L-Arg-NO pathway might have a beneficial effect on gentamicin –induced renal damage and TAS(Total Antioxidant Status), TOS (Total Oxidative Stress), MDA (Malondialdehyde), XO(Xhantine Oxidase) NO( Nitric Oxide), TNF alpha, TGF Beta, GSH (Glutathione) levels . In this purpose; six groups(n=7) of rats is planned for the study. In control group; untreated control rats will be receive saline. In GM group, GM will be inject ip,10 mg/ kg. L-arg group: rats will be received 2g/kg/day drinking water by orally ; In GM+ L-Arg group, ip,10 mg/ kg GM with 2g/kg/day L-Arg; in L-NAME group rats will be received 5 mg/100 ml/day; in L-NAME + GM group, 5 mg/100 ml/day L-NAME with ip,10 mg/ kg GM. In all groups, serum urea and creatinine levels will be measured. TAS(Total Antioxidant Status), TOS (Total Oxidative Stress), MDA (Malondialdehyde), XO(Xhantine Oxidase) NO( Nitric Oxide), TNF alpha, TGF Beta, GSH (Glutathione) levels are planned to studied in tissue homogenate. TAS, GSH as an antioxidant; MDA, XO, NO as an oxidative stress; TNF alpha and TGF Beta as an interleukin markers will be studied. Also kidney sections will be histologically studied. Conditions of chronic NO enhancement was established with L-Arg supplementation and chronic NO blockade with N-nitro-L-Arg methyl ester (L-NAME).