ACRYLONITRILE-INDUCED GASTRIC-MUCOSAL NECROSIS - ROLE OF GASTRIC GLUTATHIONE

  • 1 January 1985
    • journal article
    • research article
    • Vol. 232  (2) , 570-577
Abstract
Acrylonitrile [vinyl cyanide (VCN)] induces acute hemorrhagic focal superficial gastric mucosal necrosis or gastric erosions. The mechanism of the VCN-induced gastric erosions were studied. VCN-induced gastric lesions were 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 SH-containing compounds protected against the VCN-induced gastric necrosis and blocked the VCN-induced gastric GSH depletion. Pretreatment of rats with atropine, which blocks muscarinic receptors, protected rats against the VCN-induced gastric erosions. Depletion and/or inactivation of critical endogenous sulfhydryl groups apparently causes configurational changes of cholinergic receptors and increases agonist binding affinity, which, among other actions, leads to the causation of gastric mucosal erosions.