Gastric cytoprotection by agents altering gastric mucosal sulfhydryl compounds: role of endogenous prostaglandins.
Intragastric administration of cysteamine or diethyl maleate caused a dose-dependent reduction in the mean area of gastric lesions induced by absolute ethanol but failed to affect gastric ulcerations produced by acidified aspirin. Mucosal levels of glutathione were increased with cysteamine and reduced with diethyl maleate and did not correlate with the protective action of these agents on ethanol-induced mucosal lesions. The protective effects of these agents probably involved mucosal generation of prostaglandins, because pretreatment with indomethacin or aspirin, potent inhibitors of cyclooxygenase, partially prevented this protection. This study indicates that the mucosal generation of prostaglandins contributed, at least in part, to the gastric cytoprotection by agents altering mucosal contents of sulfhydryl compounds.
D000818:Animals; D003543:Cysteamine / Q000494:pharmacology; D015232:Dinoprostone; D011464:Epoprostenol / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000502:physiology*; D007213:Indomethacin / Q000494:pharmacology*; D007700:Kinetics; D008297:Male; D008298:Maleates / Q000494:pharmacology; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013438:Sulfhydryl Compounds / Q000378:metabolism*
D008298:Maleates; D011453:Prostaglandins; D011458:Prostaglandins E; D013438:Sulfhydryl Compounds; D000431:Ethanol; D003543:Cysteamine; D011464:Epoprostenol; C014476:diethyl maleate; D015232:Dinoprostone; D007213:Indomethacin