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

P. J. Boor, T. J. Nelson

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)679-682
Number of pages4
JournalJournal of Molecular and Cellular Cardiology
Volume14
Issue number11
DOIs
StatePublished - 1982

Fingerprint

Allylamine
Biotransformation
Acrolein
Vascular Smooth Muscle
Amines
Hazardous Substances
Mutagens
Xenobiotics
Enzymes
Smooth Muscle Myocytes
Endothelium
Hyperplasia
Coronary Vessels
Myocardium
Oxidoreductases
Fibrosis
Necrosis

Keywords

  • Acrolein
  • Allylamine
  • Biotransformation
  • Human aorta

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Cite this

Biotransformation of the cardiovascular toxin, allylamine, by rat and human cardiovascular tissue. / Boor, P. J.; Nelson, T. J.

In: Journal of Molecular and Cellular Cardiology, Vol. 14, No. 11, 1982, p. 679-682.

Research output: Contribution to journalArticle

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