Experimental assessment of the role of acetaldehyde in alcoholic cardiomyopathyReport as inadecuate

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Biological Procedures Online

, Volume 5, Issue 1, pp 1–12

Received: 03 September 2002Revised: 27 November 2002Accepted: 12 December 2002DOI: 10.1251-bpo41

Cite this article as: Aberle, N.S. & Ren, J. Biol. Proced. Online 2003 5: 1. doi:10.1251-bpo41


Alcoholism is one of the major causes of non-ischemic heart damage. The myopathic state of the heart due to alcohol consumption, namely alcoholic cardiomyopathy, is manifested by cardiac hypertrophy, compromised ventricular contractility and cardiac output. Several mechanisms have been postulated for alcoholic cardiomyopathy including oxidative damage, accumulation of triglycerides, altered fatty acid extraction, decreased myofilament Ca sensitivity, and impaired protein synthesis. Despite intensive efforts to unveil the mechanism and ultimate toxin responsible for alcohol-induced cardiac toxicity, neither has been clarified thus far. Primary candidates for the specific toxins are ethanol, its first and major metabolic product — acetaldehyde ACA and fatty acid ethyl esters. Evidence from our lab suggests that ACA directly impairs cardiac function and promotes lipid peroxidation resulting in oxidative damage. The ACA-induced cardiac contractile depression may be reconciled with inhibitors of Cytochrome P-450 oxidase, xanthine oxidase and lipid peroxidation Unfortunately, the common methods to investigate the toxicity of ACA have been hampered by the fact that direct intake of ACA is toxic and unsuitable for chronic study, which is unable to provide direct evidence of direct cardiac toxicity for ACA. In order to overcome this obstacle associated with the chemical properties of ACA, our laboratory has used the chronic ethanol feeding model in transgenic mice with cardiac over-expression of alcohol dehydrogenase ADH and anin vitro ventricular myocyte culture model. The combination of bothin vivo andin vitro approaches allows us to evaluate the role of ACA in ethanol-induced cardiac toxicity and certain cellular signaling pathways leading to alcoholic cardiomyopathy.

Indexing termsHeart Transgenic Myocyte Acetaldehyde ACA Alcohol Excitation-Contraction E-C coupling Published: February 17, 2003

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Author: Nicholas S. Aberle - Jun Ren

Source: https://link.springer.com/

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