Mechanism of ovarian disruption by neonatal DES exposure: A modified ectopic approach

Introduction Diethylstilbestrol (DES) is the classic example of an endocrine disruptor and exemplifies the damage done by xenoestrogens. DES is a non-steroidal, synthetic estrogen that was developed to supplement a woman's natural estrogen production. DES was first prescribed by physicians in 1938 for women who experienced miscarriages or premature deliveries that were believed due to insufficient levels of estrogen. However, in 1971 Herbst et al. reported the occurance 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. Preliminary studies conducted in our lab showed that neonatal exposure to DES induced morphological and functional abnormalities in the hamster ovary. In order to further investigate the neonatal DESeffects on the immature hamster ovary we exploited the cheek pouch of the Syrian golden hamster. Data collected from prior studies involving cheek pouch transplantations showed that transplanation of prepubertal ovaries while still encapsulated within the bursa hindered the process of vascularization which in turn led to the inability of the cheek pouch to sustain the implant. Our modified approach involves the dissection of ovaries out of the encapsulating bursa from control and neonatally DES-exposed donor hamsters and then transplantation of the naked ovaries into the cheek pouches of control and neonatally DES-exposed host hamsters.