This study investigated the role of oxygen free radicals in mediating renal injury after ischemia in rats. During renal ischemia, ATP is degraded to hypoxanthine, which is converted to xanthine by xanthine oxidase in the presence of oxygen, generating superoxide radicals (O₂⁻). These radicals, along with their reduction product hydroxyl radicals (OH⁻), contribute to renal injury. Superoxide dismutase (SOD), an O₂⁻ scavenger, and dimethylthiourea (DMTU), an OH⁻ scavenger, were tested for their protective effects. SOD treatment significantly reduced plasma creatinine levels and improved renal function, as evidenced by increased inulin clearance and renal blood flow. DMTU also reduced plasma creatinine and improved renal function. Allopurinol, an inhibitor of xanthine oxidase, also protected against renal injury by preventing free radical generation. The study found that reperfusion after ischemia led to lipid peroxidation, which was reduced by SOD in cortical mitochondria. These findings suggest that oxygen free radicals play a key role in renal injury after ischemia, and that scavengers like SOD and DMTU, as well as inhibitors like allopurinol, can protect renal function by reducing free radical production and damage. The study highlights the importance of oxygen free radicals in ischemic acute renal failure and supports the use of free radical scavengers as potential therapeutic agents.This study investigated the role of oxygen free radicals in mediating renal injury after ischemia in rats. During renal ischemia, ATP is degraded to hypoxanthine, which is converted to xanthine by xanthine oxidase in the presence of oxygen, generating superoxide radicals (O₂⁻). These radicals, along with their reduction product hydroxyl radicals (OH⁻), contribute to renal injury. Superoxide dismutase (SOD), an O₂⁻ scavenger, and dimethylthiourea (DMTU), an OH⁻ scavenger, were tested for their protective effects. SOD treatment significantly reduced plasma creatinine levels and improved renal function, as evidenced by increased inulin clearance and renal blood flow. DMTU also reduced plasma creatinine and improved renal function. Allopurinol, an inhibitor of xanthine oxidase, also protected against renal injury by preventing free radical generation. The study found that reperfusion after ischemia led to lipid peroxidation, which was reduced by SOD in cortical mitochondria. These findings suggest that oxygen free radicals play a key role in renal injury after ischemia, and that scavengers like SOD and DMTU, as well as inhibitors like allopurinol, can protect renal function by reducing free radical production and damage. The study highlights the importance of oxygen free radicals in ischemic acute renal failure and supports the use of free radical scavengers as potential therapeutic agents.