The effect of palm vitamin E on the healing of ethanol-induced gastric lesions andvarious biochemical parameters were investigated. The study was divided into twophases. In the first phase of the study, 42 rats of Sprague Dawley species(200–250 gm weight) were randomly divided into two groups fed with a normal diet(control) or palm vitamin E enriched diet (150mg/kg) for 3 weeks. The rats werekilled after 3 weeks of feeding. Gastric tissue contents of malondialdehyde (MDA),prostaglandin E2 and acid were measured. In the second phase of the study 42 ratswere divided into two groups. Group 1 was fed normal rat pellets (control) andgroup 2 was fed palm vitamin E enriched pellets (150mg/kg food) for 3 weeks.After 3 weeks of feeding gastric mucosal injury was induced by an orogastric tubeadministration of 0.5 ml 100% ethanol. The rats were killed at 1 hour, 4 hours and1 week after ethanol exposure for semiquantitative determination of ulcer index andgastric acid concentration. Gastric tissue MDA and muscus were measured only at1 week after ethanol exposure. In the first phase of the study we found that palmvitamin E only caused a significant reduction in gastric MDA. However, it showedno significant effects on prostaglandin E2 and gastric acid concentration. In thesecond phase of the study, the mean ulcer index of palm vitamin E supplementedgroup killed after 1 week of ethanol exposure was significantly lower compared tothe respective control. However, there was no significant difference in ulcer indexin rats killed at 1 hour and 24 hours after ethanol exposure. The gastric acidconcentration was significantly higher in the group treated with palm vitamin Ekilled 1 week after ethanol exposure compared to control. The gastric tissue MDAwas significantly lower in the palm vitamin E supplemented group compared tocontrol. There was no significant difference in gastric mucus content of the bothgroups. The ulcer healing which occurred in the presence of a high gastric acidsuggests that the effect of palm vitamin E on the healing of gastric lesions was notmediated via a reduction in gastric acid nor was it mediated through increasingprostaglandin E2 or mucus production. The most probable mechanism is viareducing lipid peroxidation as reflected by a significant decreased in gastric tissue MDA content.