Prenatal testosterone propionate and postnatal ovarian activity in the rat.

Testosterone propionate (TP) was given to rats on days 16 through 20 of pregnancy (2 mg/day). Female young had masculinized external genitalia. Sexual maturity was accelerated in TP females, despite lower weights and shorter lengths of body and tail. Placental and body weights were lower in TP females and males than in controls. The inhibiting effect of TP on postnatal growth is probably mediated by its effect on birth weight through placental damage. Ovarian cyclicity occurred upon reaching sexual maturity. In one experiment TP females were ovariectomized at 6 weeks, and given ovarian and vaginal grafts. Most of these animals showed regular cyclicity in vaginal smears between 74-100 days. Thus neither the 'early', nor the 'delayed early androgen syndrome' occurred in these experiments. This absence of effect of prenatal TP on ovarian cyclicity is attributable to a placental barrier for testosterone. When maternal plasma testosterone was raised 20-fold by exogenous TP, foetal testosterone levels remained unchanged. More detailed information was obtained when labelled testosterone was infused into a pregnant rat. Testosterone did not reach the foetus as such, but mainly as androsterone, which cannot be converted into oestrogens. This explains why prenatal TP can cause masculinization of genitalia, without 'masculinizing' the gonadotrophin secretion pattern in female rats. The latter process would presumably require oestrogenic compounds.