On the other hand, a recent report that focused on a variety of putative ED agents raises the possibility that potency as a perinatal ED agent at the whole animal level may rely on characteristics other than a given agent’s relative estrogenicity as assessed by simple in vitro assays of binding affinity to the estrogen-receptor (ER) protein and/or transactivation of ER-responsive target gene constructs. Because such unresolved questions directly relate to the mechanisms and putative consequences of endocrine disruption, they deserve continuing attention.
Most studies of the perinatal ED action of DES have assessed the later consequences in adult animals. In the hamster system, we have also assessed the early consequences in prepubertal animals. In the present study, we show that, beginning immediately following neonatal injection and progressing through the prepubertal period, overall growth of the hamster cervix was accelerated to a much greater extent by DES than by E2 treatment. A similar DES-selective effect on overall growth of the early, developing cervix was reported in the guinea pig following a prenatal treatment regimen with DES versus E2. However, something we observed in the immature hamster cervix that was not reported in the immature guinea pig study was that DES, but not E2, treatment caused precocious cor-nification of the squamous epithelium lining the ectocerv-ical lumen.