| Ethanol induces mouse spermatogenic cell apoptosis in vivo through over-expression of Fas/Fas-L, p53, and caspase-3 along with cytochrome c translocation and glutathione depletion. | |
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MedLine Citation:
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PMID: 20803734 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although it has been well established that spermatogenic cells undergo apoptosis when treated with ethanol, the molecular mechanisms behind it remain to be investigated. Adult male mice were given intra-peritoneal injection (IP) of ethanol at a dose of 3 g (15%, v/v) per kg body weight per day during the period of 14 days. Testicular androgenesis and apoptotic germ cell death, along with different interrelated proteins expression, were evaluated. Ethanol treatment induced apoptotic spermatogenic cell death with a decrease in the plasma and intra-testicular testosterone concentration. Western blot analysis revealed that repeated ethanol treatment decreased the expression of steroidogenic acute regulatory protein (StAR), 3 beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17beta-HSD); increased the expression of active caspase-3, p53, Fas and Fas-L; and led to up-regulation of Bax/Bcl-2 ratio and translocation of cytochrome c from mitochondria to cytosol in testis. It has also been shown in our study that repeated ethanol treatment led to up-regulation of caspase-3, p53, Fas, Fas-L transcripts; increase in caspase-3 and caspase-8 activities; diminution of 3beta-HSD, 17beta-HSD, and GPx activities; decrease in the mitochondrial membrane potential along with ROS generation and depletion of glutathione pool in the testicular tissue. The present study has indicated that the ethanol treatment induced apoptosis in the mouse testis through the increased expression of Fas/Fas-L and p53, up-regulation of Bax/Bcl-2 ratio, cytosolic translocation of cytochrome c along with caspase-3 activation and glutathione depletion. |
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Authors:
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Kuladip Jana; Narayan Jana; Dipak Kumar De; Sujoy Kumar Guha |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Molecular reproduction and development Volume: 77 ISSN: 1098-2795 ISO Abbreviation: Mol. Reprod. Dev. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-08-30 Completed Date: 2010-12-17 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8903333 Medline TA: Mol Reprod Dev Country: United States |
Other Details:
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Languages: eng Pagination: 820-33 Citation Subset: IM |
Copyright Information:
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(c) 2010 Wiley-Liss, Inc. |
Affiliation:
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Division of Molecular Medicine, Bose Institute, Kolkata, West Bengal, India. kuladip@bic.boseinst.ernet.in |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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17-Hydroxysteroid Dehydrogenases
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analysis 3-Hydroxysteroid Dehydrogenases / analysis Animals Apoptosis* Caspase 3 / analysis Cytochromes c / analysis Down-Regulation Ethanol / pharmacology* Fas Ligand Protein / analysis Glutathione / analysis Male Membrane Potential, Mitochondrial / drug effects Mice Phosphoproteins / analysis Proto-Oncogene Proteins c-bcl-2 / analysis Reactive Oxygen Species / analysis Spermatogenesis / drug effects* Spermatozoa / cytology, drug effects*, physiology Testis / drug effects*, metabolism Testosterone / biosynthesis, blood Tumor Suppressor Protein p53 / analysis Up-Regulation bcl-2-Associated X Protein / analysis |
| Chemical | |
Reg. No./Substance:
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0/Fas Ligand Protein; 0/Phosphoproteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Reactive Oxygen Species; 0/Tumor Suppressor Protein p53; 0/bcl-2-Associated X Protein; 0/steroidogenic acute regulatory protein; 58-22-0/Testosterone; 64-17-5/Ethanol; 70-18-8/Glutathione; 9007-43-6/Cytochromes c; EC 1.1.-/17-Hydroxysteroid Dehydrogenases; EC 1.1.-/3-Hydroxysteroid Dehydrogenases; EC 3.4.22.-/Caspase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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