Treatment of pregnant rhesus macaques with testosterone propionate: observations on its fate in the fetus.

Castrated male primates, unlike castrated male rodents, respond to exogenous estrogen by releasing gonadotropin. Although this disparity is unexplained, it may occur because the amount of testicular androgen secreted during a critical period for sexual differentiation is not sufficient to completely androgenize the anlagen of the central nervous system (CNS) in male primates. Therefore, male primates might be incompletely masculinized, and if fetal males were exposed to additional androgen during sexual development, they would no longer display the positive feedback to estrogen that usually characterizes females. Besides the development of mechanisms mediating the release of gonadotropins, questions about relationships between adult male sexual behaviors and the intensity of the androgen stimulus upon developing neural structures are of interest. We tested some of these possibilities by injecting androgen into 8 pregnant rhesus macaques from Days 40 through 50 of gestation, and we compared serum levels of testosterone (T), dihydrotestosterone (DHT), and androstenedione (delta 4) in the fetal circulation with that of 5 untreated control males. Fetal sera (both male and female) from treated pregnancies did not contain significantly greater quantities of T and DHT than sera of intact control males from untreated mothers. The maternal sera, however, contained large amounts of T (125.05 +/- 27.40 [SEM] ng/ml, n = 8) and significant elevations of DHT and delta 4 after treatment. The concentrations of delta 4 in the fetal circulation were significantly elevated (p less than 0.01) in treated fetuses compared to intact control males, probably due to the actions of the 17 beta-hydroxysteroid dehydrogenases in the placenta, the fetus, or both.(ABSTRACT TRUNCATED AT 250 WORDS)