Prenatal Estrogen Research Articles

Demasculinization of male Japanese quail by prenatal estrogen treatment

Genetic male Japanese quail were administered sex hormones or the oil vehicle on Day 10 of incubation and were caponized 3 weeks after hatching. As adults, the capons were injected with testosterone propionate daily for 2 weeks and then were tested for masculine sexual behavior in response to sexually receptive females. Males that had received as little as 2 μg of estradiol-17β in ovo failed to exhibit the head grabbing and mounting typical of the normal masculine sexual response to females. In a second experiment, this demasculinization was produced by prenatal treatment with 2 μg of estradiol-17α, estrone, estriol, or diethylstilbestrol, but not by this quantity of testosterone. These data suggest that an estrogen is the agent of behavioral demasculinization in the normal female, and that endogenous testosterone poses no difficulty for proper sexual development in the normal male.

Pathogenesis of cryptorchidism.

Cryptorchidism was induced experimentally by treating pregnant mice on the 14th day of pregnancy with 5 mg estrogen. Testes from cryptorchid and control newborn and adult mice were investigated with radioimmunoassay and electron microscopy. It was concluded that a normal Leydig cell function plays a decisive role in testicular descent. In cryptorchidism, Leydig cells at birth are atrophic. Testicular testosterone content is diminished as compared to controls. Ultrastructural alterations of Leydig cells observed in our experiments closely resemble those found in biopsies of cryptorchid patients. In male mouse offspring, prenatal estrogen injection induced not only a cryptorchidism but also Leydig cell atrophy and a permanently impaired function. Testosterone content is still significantly diminished after puberty. It is proposed therefore that an insufficiency of endocrine gonadal function of hypothalamo-pituitary origin occurring during intrauterine development is one of the main causes of cryptorchidism. An appropriate long-term therapy could diminish the high sterility rate.