This study looks at the role of
xanthine oxidase (XO) in
ischemia/reperfusion (I/R) induced intestinal mucosal damage using normal and
xanthine oxidase deficient rats.
Tungstate feeding for 3 days depleted the intestinal mucosal XO by 80%. A ligated loop of the rat small intestine (both normal and XO-deficient) was subjected to 1 h of total
ischemia followed by 5 min revascularisation. The ensuing mucosal damage was assessed by biochemical and histological studies.
Ischemia or I/R increased the XO levels in normal rats without any change in XO-deficient rats.
Myeloperoxidase (a neutrophil marker) level was increased in both group of rats but it was comparatively higher in the XO-deficient rats. Accumulation of peroxidation products such as
malondialdehyde, conjugated diene and increased production of
hydroxyl radicals by microsomes were seen after
ischemia and I/R and were similar in normal and XO-deficient rats. Studies on other parameters of peroxidation showed a decrease in
polyunsaturated fatty acids and
alpha-tocopherol, an increase in
cysteine and
cystine levels after I/R and were similar in both normal and XO-deficient rats. Histological results indicated gross morphological changes in the intestinal mucosa due to
ischemia and I/R, and the damage was more severe in XO-deficient rats. These observations suggest that
oxygen-derived
free radicals are involved in the intestinal mucosal damage during I/R and infiltrated neutrophils rather than XO may be the primary source of
free radicals under these conditions.