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of epididymal mouse sperm Lukas Ded1, Natasa Sebkova2,3, Martina Cerna2, Fatima Elzeinova1, Pavla Dostalova1,3, Jana Peknicova1 & Katerina Dvorakova-Hortova2 Author Affiliation: 1Laboratory of Reproductive Biology, Institute of Biotechnology, Academy of Sciences of the Czech Republic, v. v. i., Prague, Czech Republic 2Department of Zoology, Faculty of Science, Charles University, Prague, Czech Republic 3Departments of Cell Biology, Faculty of Science, Charles University, Prague, Czech Republic Abstract Estrogens play a crucial role in spermatogenesis, and estrogen receptor alpha knock-out male mice are infertile. Increasing evidence suggests that compounds with estrogen activity also significantly influence the sperm physiological processes. It has been demonstrated that estrogens significantly increase the speed of capacitation in vitro, however, this may lead to the reduction of reproductive potential due to the decreased ability of these sperm to undergo the acrosome reaction. Up to present the in vivo effect of estrogens on the ability of sperm to capacitate has not been investigated. Therefore, in this study, we exposed mice to 17B-estradiol (E2) at the concentration of 20 ng/ml either during puberty from the 3rd to 8th week of age (group A), or continuously from birth for a period of 12 weeks (group B) at which age the animals from both groups were sacrificed. According to our results, in vivo exposition to increased E2 concentrations caused premature sperm capacitation in the epididymis. The effect of E2, however, seems reversible, because in animals exposed only during puberty, the premature epididymal sperm capacitation is decreased compared to the continuously exposed group. After subsequent in vitro capacitation, the differences between the control and experimental groups were mainly caused by the initial difference between the numbers of capacitated sperm at the start of the capacitation. Therefore, our data implicates, that in vivo exposition to E2 under specific conditions leads to the premature capacitation of mouse sperm in epididymis with a potential negative impact on the sperm reproductive fitness in the female reproductive tract.

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