The pathogenic role of lipid peroxidation in the reperfusion injury of
the liver is still controversial. This study was performed to determi
ne whether the damage caused by oxygen free radicals during reoxygenat
ion in perfused rat hepatocytes is related to lipid peroxidation. Supe
roxide anion was detected by lucigenin-enhanced chemiluminescence. Lip
id peroxidation and cell injury were assessed by the release of malond
ialdehyde and lactic dehydrogenase. Upon reoxygenation following 2.5 h
of anoxia, isolated hepatocytes generated considerable amount of O-2-
. Following O-2- formation, a significant increase in malondialdehyde
release was measured. Cell injury was temporally delayed relative to O
-2- generation, but preceded the occurence of a significant lipid pero
xidation. Treatment with Vitamin E abolished lipid peroxidation but ha
d no effect upon superoxide anion formation and cell injury. These res
ults suggest that in perfused rat hepatocytes non-peroxidative mechani
sms are more important than peroxidative mechanisms in the pathogenesi
s of the early phases of reoxygenation injury.