This study investigates the role of oxygen free radicals in mediating renal injury after ischemia in rats. The researchers used a model of renal ischemia by performing right nephrectomy followed by 60 minutes of left renal artery occlusion. They administered superoxide dismutase (SOD), a scavenger of superoxide radical (O2-), and dimethylthiourea (DMTU), a scavenger of hydroxyl radical (OH-), to the rats before ischemia. The results showed that SOD treatment significantly reduced plasma creatinine levels, improved inulin clearance, and increased renal blood flow compared to control rats. DMTU also provided protection, as evidenced by lower plasma creatinine levels. Additionally, the xanthine oxidase inhibitor allopurinol, which prevents the generation of oxygen free radicals, was effective in protecting renal function. The study further demonstrated that reperfusion after ischemia led to lipid peroxidation, which was mitigated by SOD treatment in renal cortical mitochondria. These findings suggest that oxygen free radicals play a crucial role in renal injury after ischemia, and that scavengers of these radicals can protect renal function.This study investigates the role of oxygen free radicals in mediating renal injury after ischemia in rats. The researchers used a model of renal ischemia by performing right nephrectomy followed by 60 minutes of left renal artery occlusion. They administered superoxide dismutase (SOD), a scavenger of superoxide radical (O2-), and dimethylthiourea (DMTU), a scavenger of hydroxyl radical (OH-), to the rats before ischemia. The results showed that SOD treatment significantly reduced plasma creatinine levels, improved inulin clearance, and increased renal blood flow compared to control rats. DMTU also provided protection, as evidenced by lower plasma creatinine levels. Additionally, the xanthine oxidase inhibitor allopurinol, which prevents the generation of oxygen free radicals, was effective in protecting renal function. The study further demonstrated that reperfusion after ischemia led to lipid peroxidation, which was mitigated by SOD treatment in renal cortical mitochondria. These findings suggest that oxygen free radicals play a crucial role in renal injury after ischemia, and that scavengers of these radicals can protect renal function.