抄録
Ischemia by reduction of gastric mucosal blood flow has been proposed an explanation for the formation of stress ulcer. However, the mechanism that ischemia produces mucosal lesions remains uncertain.
Recently, the role that free radicals may plays in the ischemic-induced tissue injury have received attention.
So, in this study we investigated whether free radicals play a role in the formation of stress ulcer and furthermore whether iron plays an important role in the production of free radicals. To achieve this goal, we adapted water-immersion stress method and use various scavengers (superoxide dismutase, catalase), allopurinol, deferoxamine as chelator of ferric iron.
Allopurinol, inhibitor of xanthine oxidase, significantly reduced gastric lesions at the inhibitory rate of 80%.
When SOD and catalase were administered at the same time, the inhibitory rate was 25%. When SOD was only administered, the effect appeared at 5 hrs during its experimental course (7 hrs) . This result seemed to be related in the half time of SOD in vivo.
On the other hand, production of hydroxyl radical depends on“iron-catalysed Harber-Weiss reaction”. When deferoxamine was administered, the inhibitory rate was 45%.
These data indicated that free radicals plays a role in the formation of stress ulcer and that hydroxyl radical is more important, furthermore that ferric iron plays an important role in the production of free radical.