Mechanism of ovarian disruption by neonatal DES exposure: A further investigation into ovarian function in the hamster cheek pouch

Diethylstilbestrol (DES) is a potent, synthetic, non-steroidal estrogen that, as the classic example of an endocrine disruptor, exemplifies the damaging potential of xenoestrogens. It was widely prescribed to pregnant women between 1938 and 1971 in the belief that a supplement to natural estrogen production would prevent miscarriages or premature deliveries. However, in 1971 Herbst et al. reported the occurance of a rare form of vaginal clear cell adenocarcinoma in a group of young women who were exposed to DES in utero [1]. We use Syrian golden hamsters (Mesocricetus auratus) to investigate the phenomenon of neonatal DES-induced endocrine disruption. Our preliminary studies showed that neonatal exposure to DES induced morphological and functional abnormalities in all regions of the female hamster reproductive tract. To investigate neonatal DES-induced specifically on the hamster ovary, we exploited the animal’s cheek pouch. Our approach involved: 1) dissecting ovaries out of their encpsulating bursa after they were removed from both control and neonatally DES-exposed donor hamsters; and then 2) transplantating the naked ovaries into the cheek pouches of both control and neonatally DES-exposed host hamsters. We conducted the complete ovarian dissection procedure because prior studies suggested that transplanation of prepubertal ovaries while still encapsulated within their bursa hindered the process of vascularization which, in turn, compromised ectopic ovary function and viability.