Superoxide dismutase (SOD) scavenges
oxygen radicals that are implicated in the pathogenesis of intestinal
ischemia-reperfusion injury. The effect of intestinal
ischemia and reperfusion was investigated in transgenic mice overexpressing human Cu-Zn SOD.
Ischemia was induced by occluding the superior mesenteric artery.
Myeloperoxidase activity was determined as an index of neutrophil infiltration, and
malondialdehyde levels were measured as an
indicator of lipid peroxidation. Forty-five minutes of intestinal
ischemia followed by 4 h of reperfusion caused an increase in intestinal levels of
malondialdehyde in both nontransgenic and transgenic mice, but the concentration of
malondialdehyde was significantly greater in nontransgenic mice. Intestinal
ischemia-reperfusion also caused an increase in intestinal and pulmonary
myeloperoxidase activity in nontransgenic and transgenic mice, but the transgenic mice had significantly lower levels of
myeloperoxidase activity than nontransgenic mice. Transgenic mice had higher levels of intestinal SOD activity than nontransgenic mice. There were no significant differences in the
catalase or
glutathione peroxidase activities. In conclusion, our study demonstrates that the overexpression of SOD protects tissues from neutrophil infiltration and lipid peroxidation during intestinal
ischemia-reperfusion.