In Vivo Exposition to 17B-Estradiol Cause Premature Capacitation of Epididymal Mouse Sperm.

Abstract

Estrogens play an important role both in female and male reproductive system. In males, estrogens influence process of spermatogenesis and estrogen receptor alpha knock-out mice are infertile. Increasing evidence suggests that compounds with estrogen activity also significantly influence sperm physiological processes including capacitation. It has been demonstrated that in vitro estrogens significantly increase a speed of capacitation process however this leads in vitro to a reproductive potential reduction. During in vivo experiments, the situation could be different and in vivo exposition to estrogens and subsequent analysis of sperm capacitation was required. Therefore, in presented study, we investigated effect of in vivo exposition to 17B-estradiol (E2) in concentration 20 ng/ml on sperm capacitation in vitro. In vivo exposure to E2 was either during puberty between 3 and 8 weeks of age or postnataly for 12 weeks until animals were sacrificed. According to our results, in vivo exposition to E2 causes premature sperm capacitation already in the epididymis. The effect of E2 seems however reversible, since the end of the exposition leads to reduction in the number of capacitated epididymal sperm. After subsequent in vitro capacitation, the differences between control and experimental groups were mainly caused by initial difference between the numbers of capacitated sperm at the start of the capacitation. Therefore, our data implicates that in vivo exposition to E2 leads to premature capacitation of mouse sperm in epididymis with a potential negative impact on sperm reproductive fitness in female reproductive tract. (The work was supported by Grants of the Ministry of Education of the Czech Republic Nos. VC 1M06011 and VZ 0021620828, the Grant Agency of the Czech Republic No. 523/08/H064 and by the Institutional Research Supports AVOZ 50520701 and SVV-2012-265 206.)