Renal ischemia -reperfusion injury: contribution of nitric oxide and reactive oxygen species

ABSTRACT

The present study was undertaken to examine the effect of ischemia/reperfusion injury to the kidney on basal NO production and to define whether the antioxidants or NO precursor can modulate NO production in this model or not. Induction of renal ischemia for 60 minutes followed by 15 minutes reperfusion in adult male Wistar rats resulted into impairment of NO production as indicated by reduced serum nitrite/nitrate levels, increase in lipid peroxidation measured as malondialdehyde [MDA] and depletion of reduced glutathione [GSH] and catalase contents in rat kidney. NO precursor, L-arginine [L-ARG] as well as hydroxyl radical scavengers, dimethylthiourea [DMTU] and an iron chelator, deferoxamine [DFO] increased serum NO level and renal GSH and catalase levels and reduced renal MDA. Conversely, infusion of iron complex EDTA-FeCl3 10 minutes before ischemia exacerbated the changes in the parameters studied was induced by ischemia/reperfusion