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Reprod Toxicol. 2011 Dec;32(4):472-83. doi: 10.1016/j.reprotox.2011.09.006. Epub 2011 Sep 24.

Neonatal diethylstilbestrol exposure disrupts female reproductive tract structure/function via both direct and indirect mechanisms in the hamster.

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  • 1Department of Biological Sciences, Wichita State University, 1845 Fairmount, Wichita, KS 67260-0026, United States.

Abstract

We 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.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID:
21963885
[PubMed - indexed for MEDLINE]
PMCID:
PMC3225713
Free PMC Article

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