Showing papers by "Carol C. Cunningham published in 1994"

Differential effects of ethanol consumption on synthesis of cytoplasmic and mitochondrial encoded subunits of the ATP synthase.

Abstract: The relative concentrations of several subunits of the mitochondrial ciated with the FI (a + p and 7) are not altered in Fo.F,-ATP synthase were determined in mitochondria and submito- mitochondria from ethanol-fed animals. ln contrast, the levels of polypeptides of the FO (ATPase 6 and 8) are chondrial particles prepared from the livers of ethanol-fed and control rats. The polypeptides were separated by sodium dodecylsulfate-polyacrylamide gel electrophoresis and the stained gels were significantly de~~eased in these organelles. The data preanalyzed by densitometry for the relative concentrations of the ATP sented in this report provides additional evidence that an synthase subunits. A significant decrease in the relative concentra- ethanol-induced lesion in mitochondria1 protein syntion of the mitochondrial gene product, ATPase subunit 8, was thesis7,8 is responsible for the significant alterations in observed in mitochondria and submitochondrial particles from oxidative phosphorylation found in mitochondria from ethanol-fed animals. The relative concentration of the other mitochondrial encoded ATPase subunit, ATPase 6, was also depressed, ethanol-fed rats. Moreover, this study illustrates a difas confirmed in submitochondrial particles. In contrast, there were ferential effect of chronic ethanol consumption on cytono significant ethanol-related depressions in subunits a, 6, and OSCP plasmic and mitochondria1 protein syntheses of the ATP of the Fa. F, or the adenine nucleotide carrier in intact mitochondria. synthase subunits. These results demonstrate that ethanol consumption causes a decrease in the content of mitochondrial synthesized subunits 6 and 8 whereas no effect is exerted on the concentrations of nuclear gene products of the ATP synthase complex. Likewise, the adenine nu

Alcoholism and myocardial energy metabolism.

Abstract: A review of the effects of chronic ethanol consumption on myocardial energy metabolism in animal models reveals that alterations in cardiac function are not accompanied by changes in the levels of the high-energy metabolites, ATP, and creatine phosphate. There are minor alterations in mitochondrial ultrastructure and function that appear to be accentuated by lowered nutrient intake. Observations to date indicate that, in animal models, there is an interaction between chronic ethanol consumption and caloric deprivation in eliciting alterations in myocardial energy metabolism. Furthermore, ethanol-related ultrastructural changes and depressed mitochondrial function are much more demonstrable in liver than in heart, suggesting strongly that the myocardium is less susceptible to the deleterious effects of alcohol than is the liver.