Acrylonitrile-induced gastric mucosal necrosis: Role of gastric glutathione

B. I. Ghanayem, P. J. Boor, A. E. Ahmed

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

Abstract

Acrylonitrile [vinyl cyanide (VCN)] induces acute hemorrhagic focal superficial gastric mucosal necrosis or gastric erosions. In this report the authors have studied the mechanism of the VCN-induced gastric erosions. VCN-induced gastric lesions are coupled with a marked decrease of gastric reduced glutathione (GSH) concentration. Pretreatment of rats with various metabolic modulators (cytochrome P-450 monooxygenase and GSH) before VCN demonstrated that there is an inverse and highly significant correlation between gastric GSH concentration and the VCN-induced gastric erosions. Pretreatment of rats with sulfhydryl-containing compounds protected against the VCN-induced gastric necrosis and blocked the VCN-induced gastric GSH depletion. Furthermore, pretreatment of rats with atropine, which blocks muscarinic receptors, protected rats against the VCN-induced gastric erosions. The working hypothesis is that depletion and/or inactivation of critical endogenous sulfhydryl groups causes configurational changes of cholinergic receptors and increases agonist binding affinity, which, among other actions, leads to the causation of gastric mucosal erosions.

Original languageEnglish (US)
Pages (from-to)570-577
Number of pages8
JournalJournal of Pharmacology and Experimental Therapeutics
Volume232
Issue number2
StatePublished - 1985

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

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