Abstract: Hepatic injury after ischemia/reperfusion is attributed to thedevelopment of oxygen free radical (OFR)-mediated lipid peroxidation - aprocess that can be measured through its byproducts, specificallymalondialdehyde. The use of free radical scavengers can offer significantprotection against OFR-induced liver injury. We hypothesize that a new potentOFR scavenger, polyethylene glycol-superoxide dismutase (PEG-SOD), can inhibitOFR-mediated lipid peroxidation in hepatic ischemia/reperfusion injury. Twelve male Sprague-Dawley rats (300-350 g) were subjected toocclusion of the left and middle hepatic arteries and portal veins for 90 min,followed by 120 min reperfusion. PEG-SOD (5000 units/kg) was given intravenouslybefore vascular occlusion and again immediately upon reperfusion to six rats. Normal saline was given to the remaining six rats to be used as a controlgroup. The right hepatic lobe (used as internal control) and left hepatic lobewere harvested separately and tissue malondialdehyde was measured. A marked increase in lipid peroxide was found in the normal salinegroup after 2 h reperfusion. Treatment with PEG-SOD prevented the rise in tissuemalondialdehyde. The mean difference in the malondialdehyde between the leftand right hepatic lobes were 13.20 ± 6.35 and 1.70 ± 3.65 nmol/g in thenormal saline (control) and PEG-SOD groups, respectively. This difference wasfound to be statistically significant (P < 0.005) usingStudent's t-test. PEG-SOD can effectively attenuate hepatic ischemia/reperfusioninjury by inhibiting OFR-mediated lipid peroxidation.