Document Detail


Ethanol promotes T cell apoptosis through the mitochondrial pathway.
MedLine Citation:
PMID:  12603597     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Clinical reports suggest that acute ethanol intoxication is often associated with lymphopenia. Previously, ethanol was reported to invoke thymocyte apoptosis. We studied the effect of ethanol on T cell apoptosis. In addition, we evaluated the molecular mechanism of ethanol-induced T cell apoptosis. Human T cells harvested from healthy subjects after an alcohol drinking binge showed enhanced T cell apoptosis (before, 0.4 +/- 0.2% versus after, 19.6 +/- 2.5% apoptotic lymphocytes/field; P < 0.001). In in vitro studies, ethanol in a concentration of 50 mm and higher enhanced the apoptosis of Jurkat cells. DNA isolated from ethanol-treated Jurkat cells displayed integer multiples of 180 base pairs. Ethanol decreased Jurkat cell expression of Bcl-2, whereas ethanol increased Jurkat cell expression of Bax. Jurkat cells treated with ethanol also showed translocation of cytochrome C into cytosol. Moreover, a caspase-9 inhibitor partially inhibited ethanol-induced Jurkat cell apoptosis. In in vivo studies, after binge drinking, T cell expression of Bcl-2 also decreased. In addition, binge drinking induced the cleavage of caspase-3, suggesting activation of caspase-3 in T cells. These results suggest that ethanol promotes T cell apoptosis through the activation of intrinsic or mitochondrial pathway.
Authors:
Aditi A Kapasi; Geeta Patel; Anuj Goenka; Nilay Nahar; Neeraj Modi; Madhu Bhaskaran; Krishna Reddy; Nicholas Franki; Jaimita Patel; Pravin C Singhal
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Immunology     Volume:  108     ISSN:  0019-2805     ISO Abbreviation:  Immunology     Publication Date:  2003 Mar 
Date Detail:
Created Date:  2003-02-26     Completed Date:  2003-05-09     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0374672     Medline TA:  Immunology     Country:  England    
Other Details:
Languages:  eng     Pagination:  313-20     Citation Subset:  IM    
Affiliation:
Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, NY 11040, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Apoptosis / drug effects*
Caspase 3
Caspases / drug effects,  metabolism
Dose-Response Relationship, Drug
Ethanol / pharmacology*,  poisoning
Humans
Jurkat Cells
Male
Mitochondria / drug effects*
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
T-Lymphocytes / drug effects*,  metabolism
bcl-2-Associated X Protein
Grant Support
ID/Acronym/Agency:
R01 D 12111//PHS HHS
Chemical
Reg. No./Substance:
0/BAX protein, human; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 64-17-5/Ethanol; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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