The presence of a varicocele is associated with high levels of DNA-damage spermatozoa even in the presence of normal semen profile. The results also indicate that oxidative damage is associated with sperm DNA damage in these patients.

Although the importance of seminal plasma in the protection of spermatozoa against reactive oxygen species is well known, only a few studies have investigated its antioxidative properties and the possible relationship between infertility and plasmatic antioxidant defences. The aim of the present study was to assess the status of the total non-enzymatic antioxidant defences of human seminal plasma. Semen samples were obtained from 101 patients consulting for infertility and 15 fertile donors. A total reactive antioxidant potential (TRAP) in seminal plasma was determined by luminol-chemiluminescence. The relationship of seminal TRAP values to lipid peroxidation was also evaluated. Our results show that semen samples from fertile controls show total antioxidant capacity at higher frequency and value than equivalent samples from suspected subfertile men. This fact as well as the inverse relationship observed between antioxidant capacity and lipid peroxidation potential strongly suggest that impaired antioxidant defences may play a role in infertile disorders.

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.

This study indicates that sons of PCOS women exhibit higher body weight from early infancy. In addition, insulin resistance became evident as the subjects got older, which may place them at risk for the development of type 2 diabetes and cardiovascular disease.

AMH concentrations are increased in prepubertal sons of women with PCOS, suggesting that these boys may show an increased Sertoli cell number or function during infancy and childhood. However, this does not seem to have a major deleterious effect on sperm production.