Silver E H, Szabo S
Res Commun Chem Pathol Pharmacol. 1982 Apr;36(1):33-43.
Acrylonitrile-induced adrenal necrosis is associated with the early depletion of adrenal glutathione and elevation of adrenal dopamine. These biochemical events could result in increased susceptibility to free radical-mediated lipid peroxidation which may play a role in the pathogenesis of adrenal injury caused by acrylonitrile. In the studies reported here we found no elevation in malonaldehyde or conjugated diene concentrations of adrenal glands (or of glandular stomach and duodenal mucosa which may be other targets of acrylonitrile action) from rats given acrylonitrile. Conjugated diene concentrations in liver microsomes were significantly elevated (132%) 60 min after administration of carbon tetrachloride or 15 (38%), 30 (58%), and 60 (46%) min after injection of acrylonitrile whereas mitochondrial conjugated diene concentrations were not significantly altered by acrylonitrile. Our results suggest that while lipid peroxidation may not be involved in the pathogenesis of acrylonitrile adrenal injury it may occur in other tissues after acrylonitrile administration.
