Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In last decade it was suggested that the metabolism and toxicity of some xenobiotics may be modified by several compounds that alter the activities of microsomal oxidative and conjugating enzymes. In present study the effect of ethanol on benzene metabolism and benzene-induced hemotoxicity in pregnant rats was investigated. Pregnant female Wistar rats were exposed to benzene vapors for 6 hr/day from Days 8 through 15 of gestation at concentrations of 1500 and 3000 mg/m3 or combination ethanol and benzene at the same concentrations. Ethanol was administered intragastrically at a dose of 2.5 g/kg directly before exposure to benzene or 18 hrs before. An air-exposed or ethanol treated control rats were also studied. Before, during and after exposure blood samples for leukocyte and lymphocyte counts were obtained and urine for free phenol and conjugated phenol determinations was collected. Exposure to benzene alone decreased the maternal body weight and reduced leukocyte and lymphocyte counts in peripheral blood. Ethanol administered directly before exposure to benzene in principle had no effect on the metabolism and toxicity of benzene. It reduced the conversion of benzene to free and conjugated phenol, and protected animals from reduction of body weight and lymphopenia when was given 18 hrs before. Obtained results indicate that the early phases of benzene metabolism and its toxicity may be modified by ethanol.
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PMID:[Modification of metabolism and toxicity of benzene by ethanol in pregnant rats]. 184 23

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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PMID:Ethanol promotes T cell apoptosis through the mitochondrial pathway. 1260 97