EFFECT OF VITAMIN-E SUPPLEMENTATION ON PROSTAGLANDIN CONCENTRATIONS IN ASPIRIN-INDUCED ACUTE GASTRIC INJURY IN AGED RATS

Nonsteroidal antiinflammatory drugs (NSAIDs), such as aspirin, frequen tly cause gastric mucosal injury in the elderly. Impairment of prostag landin synthesis is a crucial step by which aspirin attenuates mucosal defense capacity. Vitamin E has been shown to decrease prostanoid con centrations, which implies an ulceropermissive effect of vitamin E. To assess the effect of vitamin E on aspirin-induced gastric injury and mucosal prostanoid concentrations, 20 male rats aged 20 mo were divide d into two groups and fed diets containing either 30 (physiologic requ irement) or 500 mg all-rac-alpha-tocopheryl acetate/kg. After 6 wk, al l rats received two intragastric doses of aspirin (1.4 mu mol/kg body wt). A third group of six animals fed the high-vitamin E diet received a vehicle solution without aspirin. Mucosal samples for vitamin E and prostaglandin E-2, 6-keto-prostaglandin F-1 alpha, and thromboxane A( 2) measurements were collected. The prevalence and degree of mucosal l esions were not significantly different among all groups. Rats fed the high-vitamin E diet had significantly higher mucosal vitamin E concen trations than rats fed the low-vitamin E diet. Mucosal concentrations of all three prostanoids were 95% lower in aspirin-treated rats than i n controls (P = 0.0001 in all instances). The high-vitamin E diet grou p had significantly lower mucosal 6-keto-prostaglandin F-1 alpha conce ntrations (P = 0.02) than thr low-vitamin E diet group, indicating dec reased prostacyclin formation, whereas concentrations of prostaglandin E-2 and thromboxane A(2) were similar in the aspirin-treated groups. Aspirin markedly reduced mucosal prostanoid concentrations in rats, wi thout apparent effects on gastric injury, whereas vitamin E supplement ation significantly reduced mucosal 6-ketoprostaglandin F-1 alpha conc entrations. Nevertheless, vitamin E supplementation did not result in more gastric injury in aspirin-treated rats than in controls.