Cellular Effects of Early Exposure to Sex Hormones and Antihormones

Developmental abnormalities of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida.

“…Both polyovular ovarian follicles and polynuclear oocytes were observed. Polyovular follicles do appear spontaneously in vertebrates and have been reported in a variety of mammals (25). Treatment of female rodents, either pre-or postnatally, with DES increases both the frequency of polyovular follicles and the number of females exhibiting this condition (25).…”

“…Or could there be subtle damage of the reproductive system that would preclude these young alligators from subsequently producing viable offspring? Recent studies suggest that exposure to low concentrations of estrogenic xenobiotic compounds during embryonic development can permanently alter the morphology and physiology of the mammalian reproductive system (14,19,20,25 (2). Woodward et al (27) found that careful handling and transport of alligator eggs avoided such mortality.…”

“…During the 6 months young alligators were raised in captivity, 9 of the original 25 neonates from Lake Apopka died, whereas 2 of the 25 Table 2). Males from Lake Apopka had a mean plasma T concentration that was not significantly different from that of females from either lake ( Table 2).…”

Neonatal estrogenic exposure suppresses PTEN-related endometrial carcinogenesis in recombinant mice

“…Simultaneously, the neonatal estrogenic agents are also well known to induce morphological alterations of the endometrium during development of the reproductive tract in mice. [30][31][32] We first hypothesized that low doses of neonatal estrogenic agents stimulate PTEN-related carcinogenesis. Contrary to our expectations, at 52 weeks of age, the incidence of CAH and adenocarcinomas of the endometrium had dramatically decreased upon neonatal estrogenic treatment in mPTEN þ /À mice.…”

“…[30][31][32] Recently, neonatal DES exposure was shown to repress the uterine expression of the abdominal B-type homeobox genes, Hoxa 10 and Hoxa 11, followed by significant loss in stromal development. 33,34 Furthermore, mice lacking either Hoxa 10 or Hoxa 11 exhibited reproductive tract phenotypes resembling those of mice treated with developmental DES exposure.…”