Experimental pharmacokinetics and toxicology of acrylonitrile.
Pharmacokinetic experiments in rats and Rhesus monkeys show that inhaled acrylonitrile is nearly completely retained and metabolized. Metabolism, according to the literature, proceeds via direct reaction of acrylonitrile with biological sulfhydryl compounds and, to a much lesser extent, via glycidonitrile as a DNA-reactive oxidative metabolite. Clinical symptoms of acute acrylonitrile intoxication are in favour of an increased parasympathetic activity. This is confirmed by increased release of acetylcholine, in presence of acrylonitrile, from isolated chicken hearts of which the N. vagus is electrically stimulated. This explains an antidotal effect of atropine. The effectiveness of N-acetyl-cysteine as an acrylonitrile antidote may be explained by decreased alkylation and inactivation of acetylcholine-esterase.
D000181:Acrylonitrile / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D002645:Chickens; D004781:Environmental Exposure; D006325:Heart Atria / Q000187:drug effects; D066298:In Vitro Techniques; D007700:Kinetics; D008253:Macaca mulatta; D008297:Male; D009570:Nitriles / Q000378:metabolism*; D051381:Rats; D014630:Vagus Nerve / Q000187:drug effects
D009570:Nitriles; D000181:Acrylonitrile