Oxygen pretreatment could induce ischemic tolerance in rat renal tissue. In the present study, the role of renal antioxidant systems in induction of this preconditioning phenomenon was investigated. Adult male rats were divided into 3 groups. The rats in O2+IR group were pretreated 1h/day for 5 days with ≤ 95% oxygen and rats in sham and IR groups with normal air. After anesthesia and right side nephrectomy, the left renal artery was closed by a clamp for 40min. Ischemia was not induced in sham group. The urine was collected for 24h and at the end of this 24h period blood and kidney samples were taken. Data are expressed as median(range). Oxygen pretreatment led to significant improvement of creatinine clearance and factional excretion of sodium. The activity of catalase (U/mgPr) in O2+IR [40(37-45)] group was significantly greater than IR [34(30-39)] group but not different from sham [40(32-53)] group. Super oxide dimutase activity in sham group was lower than other 2 groups and these 2 groups had no significant difference in this regard. Ischemia-reperfusion led to significant elevation of renal malondialdehyde level (lipid peroxidation marker, nmol/mgPr) in IR group in comparison with sham group [20(16-24) vs. 13(10-18)]; but malondialdehyde level in O2+IR [13(10-17)] group was lower than IR group and not different from sham group. In conclusion, ischemia-reperfusion leads to oxidant injury of renal tissue and oxygen pretreatment could lead to reduction of lipid peroxidation and renal ischemic damage probably due to increased catalase enzyme activity.