Corticosterone-induced attenuation of epididymal sperm fertility in rats

Stress activates the hypothalamic-pituitary-adrenal axis which results in increased circulating glucocorticoids. Corticosterone is a major glucocorticoid in rats and its excess causes a significant increase in the level of reactive oxygen species (ROS). The objective of this study was to assess the effects of different doses of corticosterone on epididymal sperm fertilizing capacity in surgically manipulated rats. Epididymides of the fertile male rats were surgically separated at the testis-caput junction. Twenty-four hours post-surgery, animals were injected (s.c.) with corticosterone at a dose of 5, 10 or 25 mg/kg/day for 7 consecutive days. On day 8, experimental male rats were cohabitated with cyclic proestrus females. Sperm-positive vaginal smear was considered as day 1 of pregnancy (p.c.). Pregnant females were laparotomized on day 8 p.c. to determine the number of implantation sites and were left until term. At parturition, the number of pups delivered was counted and compared with the number of implantation sites to determine pregnancy outcome. Results showed that only corticosterone of 25mg/kg/day for 7 consecutive days significantly decreased (p<0.05) the number of implantation sites as compared to controls. Moreover, the intrauterine embryonic loss was found to be significantly increased (p<0.01). It is concluded that corticosterone-induced attenuated fertilizing ability of the sperm and the embryonic viability that is fertilized by the damaged sperm could possibly result from an excess ROS which has yet to be verified.