Biotransformation of the cardiovascular toxin, allylamine, by rat and human cardiovascular tissue

Cardiovascular tissue has long been regarded as metabolically inert relative to other tissues, especially with regard to biotransforming xenobiotics or hazardous environmental chemicals to ultimate toxins or mutagens. Myocardium, vascular smooth muscle and endothelium, however, possess a variety of enzyme systems which synthesize or metabolize endogenous substances [8, 11] and could, theoretically, metabolize exogenous chemicals. Allylamine (3-aminopropene) is an industrial amine which affords the opportunity to test the concept that cardiovascular tissue may metabolize exogenous chemicals. In several experimental species, allylamine causes severe myocardial necrosis and fibrosis [3] accompanied by vascular smooth muscle cell hyperplasia resulting in coronary artery and aortic lesions that morphologically mimic the atherosclerotic process [4, 9, 10]. We hypothesized that allylamine is biotransformed to acrolein (allyl aldehyde) by an unknown cardiovascular deaminating enzyme, perhaps some form of amine oxidase.