The aim of the present study was to examine the effect of exposing animals to 100% oxygen instead of room air on renal function and endogenous antioxidant enzymes of the postischemic reperfused rat kidney. Superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) were determined in the homogenate of the left kidney after 45 min of ischemia, caused by clamping the left renal artery, 10 and 90 min after reperfusion while the animals breathed room air or 100% O<sub>2</sub>. The right kidney served as a control. The possible influence of trapped blood in the clamped kidney was also investigated by the use of a correction factor based on the Hb concentration in the homogenate. The results indicate that such correction is necessary as the blood adds significant antioxidant activity. The activities of all 3 enzymes after 45 min of ischemia decreased significantly in the left (ischemic) compared to the right (control) kidney, to 64% of the control levels for catalase, 58% for SOD and 49% for GPX. After 10 min of reflow, a further decrease in the activities of catalase (to 49%) and of GPX (to 29%) was found. SOD activity, however, increased to 64%. After 90 min of reperfusion, restoration toward normal levels was noticed (SOD activity increased to 70%, catalase to 76% and GPX to 58%). Breathing 100% O<sub>2</sub> resulted in a significant decrease in all enzyme activities (to 38.6% for catalase, 45% for SOD and to 27.4% for GPX). This inactivation can be explained by increased reactive oxygen species (ROS) activity during hyperoxia. However, glomerular filtration rate (GFR) and fractional excretion of sodium (FE<sub>Na</sub>) did not correlate to the enzyme activities. Thus, no increase in GFR or decrease in FE<sub>Na</sub> were seen after 90 min of reperfusion despite increase in enzyme activities above postischemic values. Moreover, these functions were not aggravated by hyperoxia as was expected. On the contrary, GFR rose slightly and FE<sub>Na</sub> decreased significantly after 90 min of reflow under 100% O<sub>2</sub>. These results may indicate that if ROS are involved in the development of postischemic damage, a different mechanism -induced by hyperoxia – may exist which protects the kidney from massive injury. Some possible mechanisms are discussed.