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Vol. 10, No. 3-4, 2001
Issue release date: May–August 2001
Section title: Paper
Biol Signals Recept 2001;10:271–282
(DOI:10.1159/000046892)

Ethanol Consumption and Liver Mitochondria Function

Cunningham C.C. · Bailey S.M.
Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, N.C., USA

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 5/24/2001

Number of Print Pages: 12
Number of Figures: 4
Number of Tables: 0

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

For additional information: http://www.karger.com/NSG

Abstract

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.


  

Author Contacts

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 cunn@wfubmc.edu

  

Article Information

Number of Print Pages : 12
Number of Figures : 4, Number of Tables : 0, Number of References : 62

  

Publication Details

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


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 5/24/2001

Number of Print Pages: 12
Number of Figures: 4
Number of Tables: 0

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

For additional information: http://www.karger.com/NSG


Copyright / Drug Dosage

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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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