Fatty Acid Ethyl Esters: Potentially Toxic Products of Myocardial Ethanol Metabolism

doi:10.1006/jmcc.1998.0812

Journal of Molecular and Cellular Cardiology

Volume 30, Issue 11, November 1998, Pages 2487-2494

https://doi.org/10.1006/jmcc.1998.0812 Get rights and content

Abstract

The chronic consumption of alcohol has proven detrimental to heart tissue and can lead to alcohol-induced heart muscle disease, a condition which may result in arrhythmias, cardiomegaly, and congestive heart failure. A search for the molecular mechanism underlying observed alcohol-induced end-organ damage, such as that seen in heart, has lead to the discovery of a nonoxidative pathway for the metabolism of alcohol in several human tissues including heart, brain, pancreas, and liver. It has been revealed that nonesterified fatty acids are esterified with ethanol to produce fatty acid ethyl esters (FAEE), neutral molecules which can accumulate in mitochondria and impair cell function. The observation that FAEEs are synthesized at high rates in the heart, and other organs that lack oxidative ethanol metabolism, provides a plausible link between the observed tissue damage, the ingestion of alcohol, and the subsequent development of alcohol-induced heart muscle disease. The synthesis of FAEEs are catalyzed by FAEE synthase enzyme, four of which have been characterized and purified to homogeneity from the human myocardium. Further analysis of these FAEE synthase enzymes opens up a new possibility to characterize and map a gene for alcohol-induced end-organ damage, such as that observed in heart and other organs. FAEEs have been found to be important metabolites of alcohol and are most commonly accumulated in those organs which are damaged by alcohol abuse, i.e. heart. It may now be important to establish a genetic link between alcohol abuse and alcohol-induced heart muscle disease in order to understand the mechanism of alcohol-induced cardiomyopathy.

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Citation Excerpt :
These patients, usually young and without evidence of heart disease, complain of palpitations, chest pain and dyspnea on weekends or after holidays: therefore, this event is called “holiday heart syndrome” [26]. Chronic alcohol abuse is able to produce myocytes hypertrophy, apoptosis and necrosis, intracellular structures dysfunction, modification of contractile proteins and calcium homeostasis, mithochondrial degeneration and fibrosis [27]. According to preclinical studies, alcohol-fed rats show a reduction of intracellular calcium concentration [28] and reduced levels of adenosine triphosphate [29] with a reduction of cardiac contractility.
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^f1: Please address all correspondence to: Dr Puran S. Bora, Department of Medicine, Division of Cardiology, Saint Louis Medical Center, 3635 Vista at Grand, USA.

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Regular ArticleFatty Acid Ethyl Esters: Potentially Toxic Products of Myocardial Ethanol Metabolism

Abstract

Regular Article
Fatty Acid Ethyl Esters: Potentially Toxic Products of Myocardial Ethanol Metabolism