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Effects of chronic ethanol ingestion upon acyl‐CoA: Carnitine acyltransferase in liver and heart
Author(s) -
Parker Sharon L.,
Thompson John A.,
Reitz Ronald C.
Publication year - 1974
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02532499
Subject(s) - ingestion , chemistry , acyl group , carnitine , cofactor , double bond , acyl coa , alcohol , clinical chemistry , coenzyme a , ethanol , biochemistry , linolenate , enzyme , acylation , medicine , endocrinology , fatty acid , biology , organic chemistry , group (periodic table) , reductase , catalysis
Abstract Chronic alcohol ingestion has been shown to cause a profound decrease in the activity of acyl‐coenzymeA:carnitine acyltransferase in the liver. Twelve diferent acyl‐coenzymes were used as substrates, and the decrease in acyltranser rates ranged from 22–60% of the control. This enzyme was not affected as drastically in the heart. Of 11 acyl‐coenzymes tested, only two resulted in significantly lower rates of acyltransfer, even though the rates were decreased with all substrates tested. The specificities of this enzyme showed that increasing the chain length of the acyl group resulted in a decreased acyltransfer when the acyl groups were either saturated, monoenoic, dienoic, or trienoic. Also, increasing the number of ethylenic bonds present in the acyl group of fatty acyl‐coenzymes of the same chain length resulted in increased rates of acyltransfer. One exception to this ethylenic bond effect was noted in the heart. Linolenate resulted in an acyl‐transfer rate lower than linoleate. Ethanol had little or no effect upon these specificities.