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Prenatal Testosterone Excess Reduces Sperm Count and Motility

Laboratory of Animal Physiology and Endocrinology (S.E.R., P.P.R.-G., M.P.R., V.H.A.), Faculty of Veterinary Sciences, University of Concepcion, Casilla 537, Chillan 3801061, Chile; Institute of Maternal and Child Research (R.S.) and Laboratory of Endocrinology and Metabolism (T.S.-P.), Department of Internal Medicine, Faculty of Medicine, University of Chile, Santiago 8320000, Chile; and Department of Pediatrics and the Reproductive Sciences Program (V.P.), University of Michigan, Ann Arbor, Michigan 48109

Address all correspondence and requests for reprints to: Professor Sergio E. Recabarren, Laboratory of Animal Physiology and Endocrinology, Faculty of Veterinary Sciences, University of Concepcion, Casilla 537, Chillan, Chile. E-mail: srecabar{at}udec.cl.

The reproductive system is extremely susceptible to insults from exposure to exogenous steroids during development. Excess prenatal testosterone exposure programs neuroendocrine, ovarian, and metabolic deficits in the female, features seen in women with polycystic ovary disease. The objective of this study was to determine whether prenatal testosterone excess also disrupts the male reproductive system, using sheep as a model system. The extent of reproductive disruption was tested by assessing sperm quantity and quality as well as Leydig cell responsiveness to human chorionic gonadotropin. Males born to mothers treated with 30 mg testosterone propionate twice weekly from d 30 to 90 and with 40 mg testosterone propionate from d 90 to 120 of pregnancy (T-males) showed a significant reduction (P < 0.05) in body weight, scrotal circumference, and sperm count compared with control males. Mean straight line velocity of sperms was also lower in T-males (P < 0.05). Circulating testosterone levels in response to the human chorionic gonadotropin did not differ between groups. These findings demonstrate that exposure to excess testosterone during fetal development has a negative impact on reproductive health of the male offspring, raising concerns relative to unintended human exposure to steroidal mimics in the environment.