Ethanol Consumption and Liver Mitochondria FunctionCunningham C.C. · Bailey S.M.
Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, N.C., USA
The mitochondrion is the subcellular organelle affected earliest during the development of alcoholic liver disease. As a result of chronic ethanol consumption mitochondrial protein synthesis is decreased significantly due to a depression in the functioning of the mitochondrial ribosome. This causes a significant decrease in the concentrations of the thirteen mitochondria gene products, all of which are components of the oxidative phosphorylation system. Consequently, there is a depression in the rate at which ATP is synthesized in hepatic mitochondria. In addition to this loss in function, hepatic mitochondria either acutely or chronically exposed to ethanol generate increased levels of reactive oxygen species (ROS). This elevation in ROS has been demonstrated in both isolated mitochondria and hepatocytes. The increase in mitochondrial ROS production accompanying acute ethanol exposure is due to mitochondrial associated reoxidation of NADH produced during ethanol and acetaldehyde metabolism. The elevation in ROS generation observed in mitochondria from chronic ethanol consumers is likely due to decreases in mitochondrial-derived electron transport components, which in turn results in higher levels of the semiquinone forms of flavin mononucleotide and ubiquinone. Both these semiquinones readily donate electrons to molecular oxygen to form superoxide.
Dr. Carol C. Cunningham
Department of Biochemistry
Wake Forest University School of Medicine
Winston-Salem, NC 27157-1016 (USA)
Tel. +1 336 716 4254, Fax +1 336 716 7671, E-Mail firstname.lastname@example.org
Number of Print Pages : 12
Number of Figures : 4, Number of Tables : 0, Number of References : 62
Biological Signals and Receptors
Vol. 10, No. 3-4, Year 2001 (Cover Date: May-August 2001)
Journal Editor: S.F. Pang, Hong Kong; P.A. Ward, Ann Arbor, Mich.; D.P. Cardinali, Buenos Aires
ISSN: 1422–4933 (print), 1422–4992 (Online)
For additional information: http://www.karger.com/journals/bsi