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\p=m-\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.

Cystinosis is an inherited metabolic disorder caused by autosomal recessive mutations in the CTNS gene leading to lysosomal cystine accumulation. The disease primarily affects the kidneys followed by extra-renal organ involvement later in life. Azoospermia is one of the unclarified complications which are not improved by cysteamine, which is the only available disease-modifying treatment. We aimed at unraveling the origin of azoospermia in cysteamine-treated cystinosis by confirming or excluding an obstructive factor, and investigating the effect of cysteamine on fertility in the Ctns À/À mouse model compared with Ellen Goossens and Elena Levtchenko contributed equally to this study.