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Science 31 January 1986:
Vol. 231. no. 4737, pp. 497 - 499
DOI: 10.1126/science.3941913
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Articles

Science, Vol 231, Issue 4737, 497-499
Copyright © 1986 by American Association for the Advancement of Science

articles

Presence of nonoxidative ethanol metabolism in human organs commonly damaged by ethanol abuse

EA Laposata and LG Lange

Acetaldehyde, the end product of oxidative ethanol metabolism, contributes to alcohol-induced disease in the liver, but cannot account for damage in organs such as the pancreas, heart, or brain, where oxidative metabolism is minimal or absent; nor can it account for the varied patterns of organ damage found in chronic alcoholics. Thus other biochemical mediators may be important in the pathogenesis of alcohol-induced organ damage. Many human organs were found to metabolize ethanol through a recently described nonoxidative pathway to form fatty acid ethyl esters. Organs lacking oxidative alcohol metabolism yet frequently damaged by ethanol abuse have high fatty acid ethyl ester synthetic activities and show substantial transient accumulations of fatty acid ethyl esters. Thus nonoxidative ethanol metabolism in addition to the oxidative pathway may be important in the pathophysiology of ethanol-induced disease in humans.


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CONCENTRATION OF FATTY ACID ETHYL ESTERS IN HAIR OF ALCOHOLICS: COMPARISON TO OTHER BIOLOGICAL STATE MARKERS AND SELF REPORTED-ETHANOL INTAKE.
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Red blood cell fatty acid ethyl esters: a significant component of fatty acid ethyl esters in the blood.
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