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Related Experiment Videos

Myocardial cell damage by fatty acid ethyl esters

P S Bora1, M A Farrar, D D Miller

  • 1Department of Internal Medicine, Saint Louis University Health Sciences Center, Missouri 63110, USA.

Journal of Cardiovascular Pharmacology
|January 1, 1996
PubMed
Summary

Fatty acid ethyl esters (FAEE), ethanol metabolites, bind to heart mitochondria and are hydrolyzed. This process leads to myocardial cell damage and dysfunction, linking ethanol abuse to heart problems.

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Area of Science:

  • Biochemistry
  • Cardiology
  • Toxicology

Background:

  • Fatty acid ethyl esters (FAEE) are myocardial metabolites of ethanol.
  • FAEE have been shown to cause mitochondrial dysfunction in vitro.

Purpose of the Study:

  • To investigate the effects of FAEE on rat heart mitochondria in vitro and in vivo.
  • To determine the binding and hydrolysis of FAEE by mitochondria.
  • To examine the histopathological changes induced by FAEE in myocardial tissue.

Main Methods:

  • In vitro studies on mitochondrial binding and hydrolysis of ethyl oleate.
  • In vivo studies involving direct myocardial transfer of [3H]oleate.
  • Histopathological examination of myocardial tissue after ethyl ester injection.

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Main Results:

  • FAEE bind to myocardial mitochondria both in vitro and in vivo.
  • Mitochondria hydrolyze FAEE to fatty acids, which uncouple oxidative phosphorylation.
  • Significant myocardial cell damage, including deformation and enlargement, observed by day 4 and increasing by day 30 post-injection.

Conclusions:

  • FAEE can damage myocardial cells and mitochondria.
  • FAEE may represent a metabolic link between ethanol abuse and myocardial dysfunction.