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dc.contributor.authorAlwis, Imala D.en_US
dc.contributor.authorMaroni, Dulce M.en_US
dc.contributor.authorHendry, Isabel R.en_US
dc.contributor.authorRoy, Shyamal K.en_US
dc.contributor.authorMay, Jeffrey V.en_US
dc.contributor.authorLeavitt, Wendell W.en_US
dc.contributor.authorHendry, William J. IIIen_US
dc.identifier.citationReproductive toxicology (Elmsford, N.Y.). 2011 Sep 24.en_US
dc.description.abstractWe assessed neonatal diethylstilbestrol (DES)-induced disruption at various endocrine levels in the hamster. In particular, we used organ transplantation into the hamster cheek pouch to determine whether abnormalities observed in the post-pubertal ovary are due to: (a) a direct (early) mechanism or (b) an indirect (late) mechanism that involves altered development and function of the hypothalamus and/or pituitary. Of the various disruption endpoints and attributes assessed: (1) some were consistent with the direct mechanism (altered uterine and cervical dimensions/organization, ovarian polyovular follicles, vaginal hypospadius, endometrial hyperplasia/dysplasia); (2) some were consistent with the indirect mechanism (ovarian/oviductal salpingitis, cystic ovarian follicles); (3) some were consistent with a combination of the direct and indirect mechanisms (altered endocrine status); and (4) the mechanism(s) for one (lack of corpora lutea) was uncertain. This study also generated some surprising observations regarding vaginal estrous assessments as a means to monitor periodicity of ovarian function in the hamster.en_US
dc.relation.ispartofseriesReproductive toxicology (Elmsford, N.Y.)en_US
dc.titleNeonatal diethylstilbestrol exposure disrupts female reproductive tract structure/function via both direct and indirect mechanisms in the hamsteren_US
dc.description.versionpeer revieweden_US
dc.rights.holderCopyright © 2011 Elsevier Inc. All rights reserved.en_US

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