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Polyethylene glycol-superoxide dismutase inhibits lipid peroxidation in hepatic ischemia/reperfusion injury
The Critical Care Forum
Wyn D Nguyen, Donald H Kim, Hasan B Alam, Haydee S Provido and John R Kirkpatrick
Department of Surgery, Washington Hospital Center, Washington, District of Columbia, USA.
Crit Care 1999 3(5):127-130 (published 23 September 1999)
Abstract
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.
Free Radicals Test kit - colour chart,/font>
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