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The Effect of Chronic Ethanol Consumption on the Lipids in Liver Mitochondria a
Author(s) -
CUNNINGHAM CAROL C.,
SPACH PRISCILLA I.
Publication year - 1987
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1987.tb48667.x
Subject(s) - gray (unit) , library science , annals , citation , medicine , history , classics , computer science , nuclear medicine
The ethanol-related alterations in hepatic mitochondrial phospholipids are primarily changes in acyl chain composition. There are no alterations in the unesterified cholesterol content in the mitochondrion, as measured by the cholesterol-phospholipid ratio. Moreover, the distribution of mitochondrial phospholipids are not changed as a result of chronic ethanol consumption. There was a significant ethanol-related decrease (18%) in the phospholipid-protein ratio in mitochondria from rats maintained on a low-fat diet, which was not observed in studies where animals were fed diets containing a higher proportion of lipid. This effect of dietary composition on the phospholipid-protein ratio was also paralleled by the interaction between diet and ethanol in influencing the phospholipid acyl composition. The alterations in acyl chain distribution indicated that ethanol consumption stimulated elongation of palmitic acid, and depressed the delta 5 desaturation step required for the formation of arachidonic acid. Elongation of palmitic acid was stimulated in studies where animals were fed diets with moderate amounts of fat, whereas depressed synthesis of arachidonate occurred more frequently, but not exclusively, in studies where low-fat diets were employed. These results indicate that there is a significant interaction between diet and ethanol in eliciting changes in hepatic mitochondrial phospholipids. The significant decrease in the linoleic acid content of cardiolipin and the more prominent ethanol-associated alterations in mitochondrial phospholipids suggest that ethanol consumption depresses the phospholipid reacylation activities associated with the mitochondrion. The above observations indicate, therefore, that the alterations occurring in mitochondrial phospholipids are influenced by ethanol-related changes in mitochondrial enzymes involved in phospholipid metabolism. In addition, alterations in the availability of fatty acids due to ethanol-related changes in microsomal elongation and desaturation activities also appear to affect the fatty acid composition of phospholipids in mitochondria from ethanol-fed animals.