During renal ischemia, ATP is degraded to hypoxanthine and xanthine oxidase is accumulated. When reperfusion develops, large amount of oxygen is supplied and superoxide radicals are generated. Free radical species were generated by a series of oxygen mediated reaction resulted in lipid peroxidation in the cellular membrane, which causes renal injury. Cyclosporin (CsA) is a potent immunosuppresant. however, one of the main adverse effects of CsA is nephrotoxicity. The mechanism of nephrotoxicity is still not fully understood. Only we proposed it as being responsible for the derangement of renal function, enhanced free radical species, vasoconstriction, ATP depletion, several vasoactive mediators. Based on the previously studied data with experimental animals, we studied a relationship between ischemia and reperfusion renal injury and cyclosporine with experimental rats. Four groups of Sprague-Dawley rats were studied: 1) a control group, only 60 minnites clamping and on day 3 is sacrified, 2) second control group, 60 minnites clamping and on day 5 is sacrified, 3) in the third and fourth group, after 60 minnites clamping, cyclosporine, 20 mg/kg/day was administrated intraperitoneally and were sacrified on day 3 and day 5, respectively. Antioxidant enzymes (SOD, Catalase), TBA-RS, GGT were measured by a specific biochemical method, and results were analyzed according to Wilcoxon rank sum test. p-value <0.05 was considered statistically significant. In cyclosporin administrated rats, GGT was elevated significantly on day 3 and day 5 (p=0.0367, p=0.0216), but SOD, Catalase, TBA-RS were not identified a significant change. In conclusion, on renal ischemia and reperfusion,cyclosporin induced renal injury is not related to free radical species, which suggests that other unknown mechanisms influence renal injury.
Adenosine Triphosphate ; Animals ; Catalase ; Constriction ; Cyclosporine* ; Free Radicals ; Hypoxanthine ; Ischemia ; Kidney ; Lipid Peroxidation ; Membranes ; Oxygen ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury* ; Reperfusion* ; Superoxides ; Vasoconstriction ; Xanthine Oxidase