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Fatty acid ethyl esters and heart disease

Alcohol Health & Research World, Summer, 1990 by Puran S. Bora, Louis G. Lange

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The normal activity of the mitochondria therefore appears to be jeopardized by the presence of both fatty acids and FAEEs (Lange and Sobel 1983a). Harm to the mitochondria and cells might occur in a cumulative manner during several years of alcohol use, eventually reaching the point where the mitochondria and the cell cannot repair themselves.

Fatty acid ethyl esters also may inhibit the normal synthesis and secretion of protein in heart muscle cells, although further work is needed to confirm this. Mair and co-workers (1990) observed such an effect following chronic exposure of liver cells to fatty acid ethyl esters.

THE ROLE OF ENZYMES

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Enzyme molecules catalyze chemical reactions, and in the human body, a specific enzyme usually will catalyze a particular reaction. The formation of FAEEs in the body is aided by an enzyme known as fatty acid ethyl ester synthase (Mogelson and Lange 1984; Mogelson et al. 1984; Lange 1982). This enzyme exists in three distinct forms in the human myocardium: Synthase I, Synthase II, and Synthase III (Bora et al. 1989a,b,c; Figure 2).

All three synthases catalyze the formation of fatty acid ethyl esters; however, Synthase I and Synthase III also catalyze the metabolsim of certain carcinogens, that is, they help to eliminate cancer-causing chemicals. Synthase I and Synthase III might also metabolize carcinogens in the heart. The effort by the synthases to metabolize both alcohol and carcinogens possibly might result in incomplete metabolism of either or both substances. Such an effect is perhaps revealed in the link between alcohol abuse and the propensity to develop tumors of the pharynx, esophagus, stomach, and liver--four organs which, in abusers, are exposed to high concentrations of alcohol (Engstrom 1977; Lieber et al. 1979).

REFERENCES

BORA, P.S., AND LANGE, L.G. Fatty acid ethyl ester, alcohol, and liver changes. In: Watson, R.R., ed. Alcohol and Drug Abuse Reviews: Liver Pathology and Drugs of Abuse. Vol. II. Clifton, NJ: Humana Press, in press a.

BORA, P.S., AND LANGE, L.G. Homogeneous Synthase I from human myocardium is a glutathione S-transferase. Annals of the New York Academy of Sciences, in press b.

BORA, P.S.; SPILBURG, C.A.; AND LANGE, L.G. Identification of a satellite fatty acid ethyl ester synthase from human myocardium as a glutathione S-transferase. Journal of Clinical Investigation 84(6):1942-1946, 1989a.

BORA, P.S.; SPILBURG, C.A.; AND LANGE, L.G. Metabolism of ethanol and carcinogens by glutathione transferases. Proceedings of the National Academy of Sciences, USA 86(12):4470-4473, 1989b.

BORA, P.S.; SPILBURG, C.A.; AND LANGE, L.G. Purification to homogeneity and characterization of major fatty acid ethyl ester synthase from human myocardium. FEBS Letters 258(2):236-239, 1989c.

ENGSTROM, J.E. Colonestal cancer and beer drinking. British Journal of Cancer Research 35:679-684, 1977.

LANGE, L.G. Nonoxidatie ethanol metabolism. Formation of fatty acid ethyl esters by cholesterol esterase. Proceedings of the National Academy of Sciences, USA 79(13):3954-3957, 1982.

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Fatty acid ethyl esters and heart disease

Alcohol Health & Research World, Summer, 1990 by Puran S. Bora, Louis G. Lange

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