The effect of cold-restraint stress on the antioxidant enzymes of the rat gastric mucosa was studied with a view to finding out their role in stress induced gastric ulceration.

Histological examination revealed stress induced extensive damage of the surface epithelial cell with lesions extending upto submucosa in some cases.

Stress causes time-dependent increase in histamine and pepsin content but decrease in acid content of the gastric fluid with the progress of ulceration (ulcer index) for two hours.

The tissue lipid peroxidation was significantly increased as evidenced by accumulation of malondialdehyde.

Since lipid peroxidation results from the generation of reactive oxygen species, stress effect was studied on some antioxidant enzymes such as superoxide dismutase, peroxidases and prostaglandin synthetase as a function of time.

The time dependent increase in stress ulcer correlates well with the concomitant increase in superoxide dismutase activity and decrease in peroxidase and prostaglandin synthetase activity.

This creates a favourable condition for accumulation of endogenous H2O2 and more reactive hydroxyl radical (OH·).

Administration of antioxidants such as reduced glutathione or sodium benzoate prior to stress causes significant decrease in ulcer index and lipid peroxidation and protection of gastric peroxidase activity suggesting the involvement of reactive oxygen species in stress induced gastric ulceration.

This is supported by the in vitro observation that OH· can also inactivate peroxidase and induce lipid peroxidation.

As prostaglandin is known to offer cytoprotection, stress-induced loss of prostaglandin synthetase activity appears to aggravate the oxidative damage caused by reactive oxygen species.