TitleEarly prenatal androgen exposure reduces testes size and sperm concentration in sheep without altering neuroendocrine differentiation and masculine sexual behavior.
Publication TypeJournal Article
Year of Publication2018
AuthorsScully, CM, Estill, CT, Amodei, R, McKune, A, Gribbin, KP, Meaker, M, Stormshak, F, Roselli, CE
JournalDomest Anim Endocrinol
Date Published2018 01
KeywordsAnimals, Female, Gonadotropin-Releasing Hormone, Luteinizing Hormone, Male, Pregnancy, Prenatal Exposure Delayed Effects, Sex Characteristics, Sexual Behavior, Animal, Sheep, Sperm Count, Spermatogenesis, Testis, Testosterone

Prenatal androgens are largely responsible for growth and differentiation of the genital tract and testis and for organization of the control mechanisms regulating male reproductive physiology and behavior. The aim of the present study was to evaluate the impact of inappropriate exposure to excess testosterone (T) during the first trimester of fetal development on the reproductive function, sexual behavior, and fertility potential of rams. We found that biweekly maternal T propionate (100 mg) treatment administered from Day 30-58 of gestation significantly decreased (P < 0.05) postpubertal scrotal circumference and sperm concentration. Prenatal T exposure did not alter ejaculate volume, sperm motility and morphology or testis morphology. There was, however, a trend for more T-exposed rams than controls to be classified as unsatisfactory potential breeders during breeding soundness examinations. Postnatal serum T concentrations were not affected by prenatal T exposure, nor was the expression of key testicular genes essential for spermatogenesis and steroidogenesis. Basal serum LH did not differ between treatment groups, nor did pituitary responsiveness to GnRH. T-exposed rams, like control males, exhibited vigorous libido and were sexually attracted to estrous females. In summary, these results suggest that exposure to exogenous T during the first trimester of gestation can negatively impact spermatogenesis and compromise the reproductive fitness of rams.

Alternate JournalDomest Anim Endocrinol
PubMed ID28843181
PubMed Central IDPMC5705409
Grant ListP51 OD011092 / OD / NIH HHS / United States
R01 OD011047 / OD / NIH HHS / United States