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Ethanol promotes T cell apoptosis through the mitochondrial pathway.

Immunology (2003-02-27)
Aditi A Kapasi, Geeta Patel, Anuj Goenka, Nilay Nahar, Neeraj Modi, Madhu Bhaskaran, Krishna Reddy, Nicholas Franki, Jaimita Patel, Pravin C Singhal
ABSTRACT

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.

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Sigma-Aldrich
Caspase-9 Inhibitor II, Cell-Permeable, The Caspase-9 Inhibitor II, Cell-Permeable controls the biological activity of Caspase-9. This small molecule/inhibitor is primarily used for Cancer applications.