Intracellular Ca2+ homeostasis and aggregation in platelets are impaired by ethanol through the generation of H2O2 and oxidation of sulphydryl groups

Rosado, JA; Nuñez, AM; Lopez, JJ; Pariente, JA; Salido, GM

HERO ID

1071144

Reference Type

Journal Article

Year

2006

Language

English

PMID

16824477

HERO ID 1071144
In Press No
Year 2006
Title Intracellular Ca2+ homeostasis and aggregation in platelets are impaired by ethanol through the generation of H2O2 and oxidation of sulphydryl groups
Authors Rosado, JA; Nuñez, AM; Lopez, JJ; Pariente, JA; Salido, GM
Journal Archives of Biochemistry and Biophysics
Volume 452
Issue 1
Page Numbers 9-16
Abstract The mechanisms involved in the effect of ethanol on Ca2+ entry and aggregability have been investigated in human platelets in order to shed new light on the pathogenesis of alcohol consumption. Ethanol (50 mM) induced H2O2 production in platelets by Ca2+-dependent and independent mechanisms. Ca2+ entry induced by ethanol was impaired by catalase. Ethanol reduced SOCE mediated by depletion of the 2,5-di-(tert-butyl)-1,4-hydroquinone (TBHQ)-sensitive acidic stores but enhances SOCE regulated by the dense tubular system. This effect was abolished by treatment with catalase or the sulphydryl group reducing agent dithiotreitol (DTT). Similarly, the anti-aggregant effect of ethanol was prevented by platelet treatment with catalase or DTT. In conclusion we provide considerable evidence that ethanol alters Ca2+ entry and reduces thrombin-induced aggregation as a result of the generation of H2O2 and the oxidation of sulphydryl groups in human platelets.
Doi 10.1016/j.abb.2006.05.011
Pmid 16824477
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Is Qa No