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Am J Physiol Gastrointest Liver Physiol 289: G1115-G1123, 2005. First published July 14, 2005; doi:10.1152/ajpgi.00193.2005
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LIVER AND BILIARY TRACT

Ethanol feeding enhances age-related deterioration of the rat hepatic mitochondrion

Alan Cahill, Stuart Hershman, Adrian Davies, and Peter Sykora

Thomas Jefferson University, Philadelphia, Pennsylvania

Submitted 29 April 2005 ; accepted in final form 27 June 2005

Chronic ethanol feeding damages the hepatic mitochondrion by increasing mitochondrial DNA (mtDNA) oxidation, lowering mtDNA yields and impairing mitochondrial respiration. These effects are also seen during aging. By employing a 21-day chronic feeding regimen, we investigated the effects of ethanol consumption on mtDNA content and mitochondrial respiration in 2-, 12-, and 24-mo-old male rats. Aging resulted in decreased mtDNA content, increased mtDNA damage (as indicated by inhibition of Taq polymerase progression), and a decline in state 3 respiration; effects that were further exacerbated by ethanol feeding. Additionally, ethanol consumption caused an increase in the levels of citrate synthase while not impacting mitochondrial protein content. In conclusion, ethanol and aging combine to cause deterioration in the structural and functional integrity of the hepatic mitochondrion. The additive effects of aging and ethanol feeding may have serious consequences for hepatic energy metabolism in aged animals, and their detrimental combination may serve as one of the molecular mechanisms underlying the progression of alcoholic liver disease.

mitochondrial DNA; respiration; polymerase-blocking lesions; citrate synthase


Address for reprint requests and other correspondence: A. Cahill, Dept. of Pathology, Anatomy, and Cell Biology, Thomas Jefferson Univ., 1020 Locust St., Philadelphia, PA 19107 (e-mail: alan.cahill{at}jefferson.edu)






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