Polyethylene glycol-superoxide dismutase inhibits lipid peroxidation in hepatic ischemia/reperfusion injury

Background:
Hepatic injury after ischemia/reperfusion is attributed to the
development of oxygen free radical (OFR)-mediated lipid peroxidation - a
process that can be measured through its byproducts, specifically
malondialdehyde. The use of free radical scavengers can offer significant
protection against OFR-induced liver injury. We hypothesize that a new potent
OFR scavenger, polyethylene glycol-superoxide dismutase (PEG-SOD), can inhibit
OFR-mediated lipid peroxidation in hepatic ischemia/reperfusion injury.

      Methods:
      Twelve male Sprague-Dawley rats (300-350 g) were subjected to
            occlusion 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 intravenously
            before vascular occlusion and again immediately upon reperfusion to six rats.
            Normal saline was given to the remaining six rats to be used as a control
            group. The right hepatic lobe (used as internal control) and left hepatic lobe
            were harvested separately and tissue malondialdehyde was measured.


      Results:
      A marked increase in lipid peroxide was found in the normal saline
            group after 2 h reperfusion. Treatment with PEG-SOD prevented the rise in tissue
            malondialdehyde. The mean difference in the malondialdehyde between the left
            and right hepatic lobes were 13.20 ± 6.35 and 1.70 ± 3.65 nmol/g in the
            normal saline (control) and PEG-SOD groups, respectively. This difference was
            found to be statistically significant (P < 0.005) using
            Student's t-test.


      Conclusions:
      PEG-SOD can effectively attenuate hepatic ischemia/reperfusion
            injury by inhibiting OFR-mediated lipid peroxidation.