Sodium nitroprusside and L-arginine attenuates ferric nitrilotriacetate-induced oxidative renal injury in rats.

摘要: Abstract The role of nitric oxide (NO) in acute renal failure (ARF) is debatable. In the present study, we investigated effect administration NO donor, Sodium nitroprusside (SNP), l -Arginine ( -Arg) and synthase inhibitor, N(omega)- -arginine methyl ester -NAME) Fe-NTA induced toxicity. Rats were pretreated with SNP (2.5 mg/kg i.p), -Arg (125 mg/kg, i.p.) -NAME (10 mg/kg, prior to (8 mg iron/kg body weight, determine urea creatinine levels along biochemical analysis oxidative stress. markedly increased BUN serum level which was coupled a marked lipid peroxidation, decreased reduced glutathione total rat kidneys significant morphological alterations. It also resulted increase tumor necrosis factor-α (TNF-α) serum. Concomitant treatment significantly levels, peroxidation manner, restored glutathione, normal morphology. Pretreatment attenuated TNF-α manner. Prior reversed protective effects produced by -Arg. Present findings strongly suggest that plays pathophysiology iron-induced donors can be valuable ARF.