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Diethylstilbestrol Versus Estradiol as Neonatal Disruptors of the Hamster (Mesocricetus auratus) Cervix¹

Department of Biological Sciences,³ Wichita State University, Wichita, Kansas 67260 Division of Genetic and Reproductive Toxicology,⁴ National Center for Toxicological Research,Jefferson, Arkansas 72079 Daniel M. Sheehan and Associates,⁵ Little Rock, Arkansas 72202

The synthetic estrogen diethylstilbestrol (DES) is an established, estrogenic endocrine disruptor (ED). The Syrian golden hamster (Mesocricetus auratus) offers some unique advantages as an experimental system to investigate the perinatal ED action of DES and other estrogenic EDs. Previous analyses regarding the consequences of neonatal administration (100 µg) of DES versus estradiol-17ß (E₂) showed that DES had a more potent disruptive effect on morphogenesis and gene expression in the uterus, oviduct, and ovary as well as in the testis and male accessory organs. The objectives of the present study were to describe the histopathological consequences of the two neonatal treatment regimens in the hamster cervix and to compare them with our previous observations in the hamster uterus. As previously found in the hamster uterus, DES was more potent than E₂ as a neonatal disruptor of the hamster cervix in prepubertal animals and in ovarian-intact adult animals. However, the cervix-versus-uterus scenario diverged in animals that were ovariectomized prepubertally and then chronically stimulated with natural estrogen (E₂). We confirmed previous observations that neonatal exposure to DES, but not to E₂, permanently alters estrogen responsiveness in the adult hamster uterus, but neither neonatal treatment regimen affected estrogen responsiveness in the adult hamster cervix. These results suggest that an unidentified ovarian factor influences the extent of neonatal DES-induced disruption of the cervix, but not of the uterus, in hamsters.

¹ Supported by U.S. Public Health Service grants CA60250 and P20 RR16475 (BRIN program of the National Center for Research Resources), the Flossie E. West Memorial Foundation, and the U.S. Food and Drug Administration.

² Correspondence: William J. Hendry III, Department of Biological Sciences, Wichita State University, 1845 Fairmount, Wichita, KS 67260- 0026. FAX: 316 978 3772; william.hendry{at}wichita.edu

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