Alcohol
Volume 26, Issue 2 , Pages 65-67, February 2002

Methionine synthase:☆☆☆

a possible prime site of the ethanolic lesion in liver

  • Anthony J. Barak

      Affiliations

    • Corresponding Author InformationCorresponding author. Tel.: +1-402-346-8800, Ext. 3547; fax: +1-402-449-0604. Requests for reprints should be addressed to Anthony J. Barak, Ph.D., Liver Study Unit (151), VA Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105, USA.(A.J. Barak)
    • ,
  • Harriet C. Beckenhauer
    • ,
  • Dean J. Tuma

Liver Study Unit and V.A. Alcohol Research Center, Department of Veterans Affairs Medical Center, Omaha, NE 68105, USA

Received 13 August 2001; received in revised form 6 November 2001; accepted 10 November 2001.

Abstract 

Among the most important pathways for liver integrity in the body are the two that synthesize methionine and S-adenosylmethionine (SAM) through methylation of homocysteine. Results of studies in this laboratory have demonstrated ethanolic inhibition of one of these pathways catalyzed by methionine synthetase. It has been shown elsewhere that alcohol per se does not inhibit the enzyme, but that the metabolite of ethanol, acetaldehyde, is responsible through the formation of an inhibiting covalent adduct. Because hepatic SAM has been shown to be essential in the transport of fat from the liver, avoiding steatosis and further liver damage, it is entirely feasible that this repression of methionine synthase is an important site of the injurious action of alcohol metabolism in the liver. This loss of activity is particularly important in human beings who cannot produce methionine and SAM by means of the alternate pathway mediated by betaine:homocysteine:transmethylase, because of the lack of production of the betaine substrate for this enzyme.

Keywords:  Methionine synthetase, Liver, Lesion, Ethanol, S-adenosylmethionine

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☆ Editor's Note: This Mini-Review Article, as with all submissions to Alcohol, was subjected to peer-review. As with all other published material in Alcohol, the authors of this Mini-Review Article satisfactorily addressed the concerns of the reviewers. Therefore, this Mini-Review Article should be considered as a peer-reviewed publication.

☆☆ Editor: T.R. Jerrells

PII: S0741-8329(01)00201-4

Alcohol
Volume 26, Issue 2 , Pages 65-67, February 2002

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