Nonsteroidal anti-inflammatory drugs and their adverse effects on the gastric mucosa are yet another set of unresolved medical problems. This study examined the effects of various antioxidants on several gastric parameters after a single exposure to indomethacin. Forty-eight male rats of the Sprague-Dawley (200-250 g) strain were randomly divided to receive a single antioxidant (tocopherol, tocotrienol, or ubiquinone) or a combination of two (tocopherol-tocotrienol, tocopherol-ubiquinone or tocotrienol-ubiquinone) for 28 days. The rats were then challenged with a single dose of indomethacin and killed six hours later. Findings showed that the severity of gastric lesions was comparable in all groups. Only groups that received a combination of antioxidants exhibited reduced lipid peroxidation compared with all other groups (p < 0.05). The combination groups had a higher level of gastric prostaglandin E2 (PGE2) content compared with all other groups (p < 0.05). There was no significant difference among the groups in the gastric acid concentration and the glutathione/oxidized glutathione (GSH/GSSG) ratio. We conclude that although supplementation of these antioxidants in combination had desirable effects on lipid peroxidation and gastric PGE2 level, they did not reduce the lesions produced by indomethacin.
The effect of palm vitamin E on the healing of ethanol-induced gastric lesions and various biochemical parameters were investigated. The study was divided into two phases. 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 (150 mg/kg) for 3 weeks. The rats were killed 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 rats were divided into two groups. Group 1 was fed normal rat pellets (control) and group 2 was fed palm vitamin E enriched pellets (150 mg/kg food) for 3 weeks. After 3 weeks of feeding gastric mucosal injury was induced by an orogastric tube administration of 0.5 ml 100% ethanol. The rats were killed at 1 hour, 4 hours and 1 week after ethanol exposure for semiquantitative determination of ulcer index and gastric acid concentration. Gastric tissue MDA and mucus were measured only at 1 week after ethanol exposure. In the first phase of the study we found that palm vitamin E only caused a significant reduction in gastric MDA. However, it showed no significant effects on prostaglandin E2 and gastric acid concentration. In the second phase of the study, the mean ulcer index of palm vitamin E supplemented group killed after 1 week of ethanol exposure was significantly lower compared to the respective control. However, there was no significant difference in ulcer index in rats killed at 1 hour and 24 hours after ethanol exposure. The gastric acid concentration was significantly higher in the group treated with palm vitamin E killed 1 week after ethanol exposure compared to control. The gastric tissue MDA was significantly lower in the palm vitamin E supplemented group compared to control. There was no significant difference in gastric mucus content of the both groups. The ulcer healing which occurred in the presence of a high gastric acid suggests that the effect of palm vitamin E on the healing of gastric lesions was not mediated via a reduction in gastric acid nor was it mediated through increasing prostaglandin E2 or mucus production. The most probable mechanism is via reducing lipid peroxidation as reflected by a significant decreased in gastric tissue MDA content.