Showing papers by "Carol C. Cunningham published in 1990"
TL;DR: The bovine heart F0F1-ATPase preparation has been further delipidated and the enzyme appears to have high affinity for cardiolipin exclusively, since PC (a prominent inner membrane lipid), phosphatidyl serine (an acidic phospholipid), and phosphatids were not immobilized (rendered NMR-invisible) when added to the delipidation preparation.
227 citations
TL;DR: It appears that the decreased levels of mitochondria-derived polypeptide components of the oxidative phosphorylation system are primarily responsible for the depression in both the rate and efficiency of ATP synthesis.
Abstract: Chronic ethanol consumption results in a generalized depression in hepatic mitochondrial energy metabolism. Both the rate and efficiency of ATP synthesis via the oxidative phosphorylation system are decreased. Alterations in the activities of several components of the oxidative phosphorylation system contribute to the overall decrease in the capacity for ATP synthesis. There appears to be no alteration in any particular component which is rate-limiting. Although changes in membrane lipids may play a minor role, it appears that the decreased levels of mitochondria-derived polypeptide components of the oxidative phosphorylation system are primarily responsible for the depression in both the rate and efficiency of ATP synthesis. The concentrations of these mitochondrial gene products are lowered due to effects of chronic ethanol consumption on the mitochondrial translational process.
171 citations
TL;DR: Liver mitochondria from rats fed ethanol chronically demonstrate an impaired ability to incorporate methionine into polypeptide products in vitro, and the steady-state concentration of each of the mitochondrial gene products is decreased in ethanol-fed rats, suggesting an ethanol-induced coordinate depression of mitochondrial protein synthesis.
80 citations