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dc.contributor.authorHendry, William J. IIIen_US
dc.contributor.authorWeaver, Benjamin P.en_US
dc.contributor.authorNaccarato, Teran R.en_US
dc.contributor.authorKhan, Shafiq A.en_US
dc.date.accessioned2012-01-24T17:49:29Z
dc.date.available2012-01-24T17:49:29Z
dc.date.issued2006-04en_US
dc.identifier16439099en_US
dc.identifierES 10232/ G12 RR03062/ P20 RR016475en_US
dc.identifier8803591en_US
dc.identifierS0890-6238(05)00266-2en_US
dc.identifier.citationReproductive toxicology (Elmsford, N.Y.). 2006 Apr; 21(3): 225-40.en_US
dc.identifier.issn0890-6238en_US
dc.identifier.urihttp://dx.doi.org/10.1016/j.reprotox.2005.09.014
dc.identifier.urihttp://hdl.handle.net/10057/4174
dc.descriptionClick on the DOI link below to access the article (may not be free).en_US
dc.description.abstractThe synthetic estrogen diethylstilbestrol (DES) is now recognized as the prototypical endocrine disruptor. Using a hamster experimental system, we performed a detailed temporal assessment of how neonatal DES-induced disruption progresses in the testis compared to the seminal vesicle. Both morphological and Western blot analyses confirmed that neonatal DES exposure alters androgen responsiveness in the male hamster reproductive tract. We also determined that the disruption phenomenon in the male hamster is manifest much earlier in the seminal vesicle than in the testis and that testis disruption often occurs differently between the pair of organs in a given animal. In the neonatally DES-exposed seminal vesicle, histopathological effects included: (1) general atrophy, (2) lack of exocrine products, (3) epithelial dysplasia, (4) altered organization of stromal cells and extracellular matrix, and (5) striking infiltration with polymorphonuclear leukocytes. Also, the morphological disruption phenomenon in the seminal vesicle was accompanied by a range of up-regulation and down-regulation responses in the whole organ levels of various proteins.en_US
dc.description.sponsorshipNIEHS NIH HHS/ NCRR NIH HHS/ NCRR NIH HHSen_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.relation.ispartofseriesReproductive toxicology (Elmsford, N.Y.)en_US
dc.sourceNLMen_US
dc.subjectResearch Support, N.I.H., Extramuralen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Newbornen_US
dc.subject.meshCricetinaeen_US
dc.subject.meshDiethylstilbestrol/toxicityen_US
dc.subject.meshEndocrine Disruptors/toxicityen_US
dc.subject.meshMaleen_US
dc.subject.meshOrgan Size/drug effectsen_US
dc.subject.meshProteins/analysisen_US
dc.subject.meshSeminal Vesicles/drug effectsen_US
dc.subject.meshTestis/drug effectsen_US
dc.subject.meshTestosterone/blooden_US
dc.subject.meshTime Factorsen_US
dc.subject.meshProteins/metabolismen_US
dc.subject.meshSeminal Vesicles/metabolismen_US
dc.subject.meshSeminal Vesicles/pathologyen_US
dc.subject.meshTestis/pathologyen_US
dc.titleDifferential progression of neonatal diethylstilbestrol-induced disruption of the hamster testis and seminal vesicleen_US
dc.typeArticleen_US
dc.description.versionpeer revieweden_US
dc.rights.holderCopyright © 2006, Elsevieren_US


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