Isolated, perfused rat livers from Sprague-Dawley rats were subjected to 60 min low flow ischemia-30 min reperfusion (37°C). The effluent perfusate activities of lactate dehydrogenase (LDH) and purme nucleoside phosphorylase (PNP) were measured as markers of parenchyma! and endothelial cell injury; respectively. In addition, tissue and effluent perfusate activities of xanthine dehydrogenase (XDH) and oxidase (XOD) were determined. After 60 min low flow ischemia-30 min reperfusion there was a slight increase in tissue %XOD activity (18.6 ± 0.2%) as compared to control (15.5 ± 0.8%). Effluent perfusate XOD activity during reperfusion was not elevated over pre-ischemia levels. Allopurmol pretreatment (200 mg/kg, i.p.; 20 and 2 hr before experiments) enhanced the release of LDH and PNP into the effluent perfusate during reperfusion after 60 min low flow ischemia as compared to controls, suggesting that inhibition of XOD increased the susceptibility of liver to reperfusion injury. Livers exposed to uric acid (250 μM) exhibited less effluent perfusate LDH and PNP activities during reperfusion after 60 min low flow ischemia as compared to controls; whereas hypoxanthine and xanthine (250 μM) had no effect. XDH/XOD may protect liver against oxidative injury by forming uric acid in low flow ischemia-reperfusion.