Gastric mucosal protection by agents altering gastric mucosal sulfhydryls. Role of endogenous prostaglandins.
Intragastric administration of sulfhydryl-containing cysteamine or sulfhydryl-oxidizing diethylmaleate caused a dose-dependent reduction in the mean area of gastric lesions induced by absolute ethanol. The protective effects of these agents are abolished by the sulfhydryl blocker N-ethylmaleimide, while indomethacin, a potent inhibitor of cyclooxygenase, caused only about 50% reduction in this protection. This study indicates that mucosal generation of prostaglandins contributes to the gastric cytoprotection by these agents administered intragastrically, but endogenous sulfhydryls are also involved in the gastric mucosal protection by sulfhydryl-containing or sulfhydryl-oxidizing compounds.
D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology*; D003543:Cysteamine / Q000494:pharmacology; D015232:Dinoprostone; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008298:Maleates / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000517:prevention & control*; D013438:Sulfhydryl Compounds / Q000032:analysis*
D000897:Anti-Ulcer Agents; D008298:Maleates; D011453:Prostaglandins; D011458:Prostaglandins E; D013438:Sulfhydryl Compounds; D003543:Cysteamine; C014476:diethyl maleate; D015232:Dinoprostone; D007213:Indomethacin