Activation and impairment of platelet function in vitro by fatty acid ethyl ester, a nonoxidative ethanol metabolite

Effect of fatty acid ethyl esters on human platelets

Raneem O. Salem, Michael Laposata

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: The goal of this study was to investigate the effect of fatty acid ethyl esters (FAEE), nonoxidative metabolites of ethanol, on platelet function. We hypothesized that FAEE increase the risk of bleeding by producing an alteration in platelet membrane structure or function. Methods: Isolated human platelets incubated with FAEE were prepared and multiple assays for platelet activation were performed; β-thromboglobulin release from platelet granules, platelet aggregation, arachidonate release from phospholipids, and intracellular cyclic AMP (cAMP) levels. We examined also the combined effect of epinephrine and FAEE on platelet aggregation. Results: FAEE induced platelet shape change, release of α granules and release of arachidonate from phospholipids without an increase in eicosanoid production and decreased cAMP levels. The platelets did not aggregate in response to FAEE alone, but did shorten the time to maximum aggregation with epinephrine. Conclusion: These studies show that FAEE potentiate platelet activation but do not induce aggregation, presumably because they do not stimulate thromboxane A2 production.

Original languageEnglish (US)
Pages (from-to)2079-2088
Number of pages10
JournalAlcoholism: Clinical and Experimental Research
Volume30
Issue number12
DOIs
StatePublished - Dec 2006
Externally publishedYes

Fingerprint

Platelet Activation
Metabolites
Platelets
Esters
Ethanol
Fatty Acids
Blood Platelets
Chemical activation
Agglomeration
Platelet Aggregation
Cyclic AMP
Epinephrine
Phospholipids
Thromboxane A2
Eicosanoids
In Vitro Techniques
Membrane structures
Hemorrhage
Assays
Membranes

Keywords

  • Alcohol
  • Arachidonic Acid Release
  • cAMP
  • Ethanol
  • Fatty Acid Ethyl Esters
  • Lipid
  • Platelet Aggregation

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology

Cite this

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title = "Activation and impairment of platelet function in vitro by fatty acid ethyl ester, a nonoxidative ethanol metabolite: Effect of fatty acid ethyl esters on human platelets",
abstract = "Background: The goal of this study was to investigate the effect of fatty acid ethyl esters (FAEE), nonoxidative metabolites of ethanol, on platelet function. We hypothesized that FAEE increase the risk of bleeding by producing an alteration in platelet membrane structure or function. Methods: Isolated human platelets incubated with FAEE were prepared and multiple assays for platelet activation were performed; β-thromboglobulin release from platelet granules, platelet aggregation, arachidonate release from phospholipids, and intracellular cyclic AMP (cAMP) levels. We examined also the combined effect of epinephrine and FAEE on platelet aggregation. Results: FAEE induced platelet shape change, release of α granules and release of arachidonate from phospholipids without an increase in eicosanoid production and decreased cAMP levels. The platelets did not aggregate in response to FAEE alone, but did shorten the time to maximum aggregation with epinephrine. Conclusion: These studies show that FAEE potentiate platelet activation but do not induce aggregation, presumably because they do not stimulate thromboxane A2 production.",
keywords = "Alcohol, Arachidonic Acid Release, cAMP, Ethanol, Fatty Acid Ethyl Esters, Lipid, Platelet Aggregation",
author = "Salem, {Raneem O.} and Michael Laposata",
year = "2006",
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doi = "10.1111/j.1530-0277.2006.00256.x",
language = "English (US)",
volume = "30",
pages = "2079--2088",
journal = "Alcoholism: Clinical and Experimental Research",
issn = "0145-6008",
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}

TY - JOUR

T1 - Activation and impairment of platelet function in vitro by fatty acid ethyl ester, a nonoxidative ethanol metabolite

T2 - Effect of fatty acid ethyl esters on human platelets

AU - Salem, Raneem O.

AU - Laposata, Michael

PY - 2006/12

Y1 - 2006/12

N2 - Background: The goal of this study was to investigate the effect of fatty acid ethyl esters (FAEE), nonoxidative metabolites of ethanol, on platelet function. We hypothesized that FAEE increase the risk of bleeding by producing an alteration in platelet membrane structure or function. Methods: Isolated human platelets incubated with FAEE were prepared and multiple assays for platelet activation were performed; β-thromboglobulin release from platelet granules, platelet aggregation, arachidonate release from phospholipids, and intracellular cyclic AMP (cAMP) levels. We examined also the combined effect of epinephrine and FAEE on platelet aggregation. Results: FAEE induced platelet shape change, release of α granules and release of arachidonate from phospholipids without an increase in eicosanoid production and decreased cAMP levels. The platelets did not aggregate in response to FAEE alone, but did shorten the time to maximum aggregation with epinephrine. Conclusion: These studies show that FAEE potentiate platelet activation but do not induce aggregation, presumably because they do not stimulate thromboxane A2 production.

AB - Background: The goal of this study was to investigate the effect of fatty acid ethyl esters (FAEE), nonoxidative metabolites of ethanol, on platelet function. We hypothesized that FAEE increase the risk of bleeding by producing an alteration in platelet membrane structure or function. Methods: Isolated human platelets incubated with FAEE were prepared and multiple assays for platelet activation were performed; β-thromboglobulin release from platelet granules, platelet aggregation, arachidonate release from phospholipids, and intracellular cyclic AMP (cAMP) levels. We examined also the combined effect of epinephrine and FAEE on platelet aggregation. Results: FAEE induced platelet shape change, release of α granules and release of arachidonate from phospholipids without an increase in eicosanoid production and decreased cAMP levels. The platelets did not aggregate in response to FAEE alone, but did shorten the time to maximum aggregation with epinephrine. Conclusion: These studies show that FAEE potentiate platelet activation but do not induce aggregation, presumably because they do not stimulate thromboxane A2 production.

KW - Alcohol

KW - Arachidonic Acid Release

KW - cAMP

KW - Ethanol

KW - Fatty Acid Ethyl Esters

KW - Lipid

KW - Platelet Aggregation

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JO - Alcoholism: Clinical and Experimental Research

JF - Alcoholism: Clinical and Experimental Research

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