The Role of Oxygen Free Radicals in Acute Renal Failure Complicating Obstructive Jaundice: An Experimental Study

Oxydant injury is considered to be an important mechanism in the pathophysiology of acute renal failure. It has been thought that decrease in extracellular and intracellular fluid and endotoxemia seen in obstructive jaundice may cause an increase in production of oxygen free radicals and impairment in antioxydant defense mechanism. This study is designed to investigate the possible role of oxydant injury in renal failure seen in jaundiced patients. In this study, 28 rats were divided into four groups: Control(C) (N=7); Renal ischemia (RI) (N=7); Obstructive jaundice+renal ischemia (OJ+RI) (N=7); Obstructive jaundice (OJ) (N=7). All groups were compared with each other according to renal failure findings and enzyme activities, such as Xanthine oxidase (XOD), Superoxide Dismutase (SOD) and Catalase in renal cortex and Glutathione Peroxidase (GSH-Px), in blood at 3rd day after ischemia and reperfusion. Renal failure findings monitored by blood urea and creatinine levels, seemed more evident in OJ+RI than RI group (p <0.05). When compared with RI, in OJ+RI group, increase in XOD activity at 3rd day was statistically significant [0.259 ±0.01 U/g (tissue) and 0.362±0.03 U/g (tissue) respectively] (p <0.05). SOD and GSH-Px activities of each ischemic group at 3rd day were decreased compared to non-ischemic groups. This fall was significant (p <0.05). But there was no statistical difference between jaundiced and non-jaundiced groups. Alterations in catalase activities also had no statistical significance. These findings may suggest that the injury induced by oxygen free radicals at re-oxygenation of tissue after ischemia may also play a role in the pathogenesis of acute renal failure developed in obstructive jaundice.