In vivo exposure to 17B-estradiol triggers premature sperm capacitation in cauda epididymis

0394635 - BTÚ 2014 CZ eng A - Abstract
Děd, Lukáš - Šebková, N. - Černá, M. - Elzeinová, Fatima - Dostálová, Pavla - Pěknicová, Jana - Dvořáková-Hortová, K.
In vivo exposure to 17B-estradiol triggers premature sperm capacitation in cauda epididymis.
Book of abstracts. Praha: Biotechnologický ústav, 2013 - (Pěknicová, J.). s. 20-21
[XIX. Symposium imunologie a biologie reprodukce s mezinárodní účastí. 23.05.2013-25.05.2013, Třešť]
R&D Projects: GA ČR(CZ) GA523/09/1793
Institutional research plan: CEZ:AV0Z50520701
Keywords : Estrogen * Sperm capacitation * 17β-estradiol
Subject RIV: DN - Health Impact of the Environment Quality

Estrogens play a crucial role in spermatogenesis, and estrogen receptor alpha knock-out male mice are infertile. 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 (N=24) to 17B-estradiol (E2) at the concentration of 20 ng/ml either during puberty from the 4th to 7th week of age (N=8), or continuously from birth for a period of 12 weeks (N=8) at which age the animals from both groups were sacrificed. The capacitation status of epididymal and testicular sperm was analysed by TyrP antibody (immunofluoescence and western blot) and CTC assay. According to our results, in vivo exposure to increased E2 concentrations caused premature sperm capacitation in the epididymis. The effect of E2, however, seems reversible, because after the termination of the exposure, premature epididymal sperm capacitation is decreased in puberty treated animals. Furthermore, the changes in epididymal sperm capacitation status detected by TyrP and CTC positively correlate with plasma levels of E2 and the expression of the estrogen-dependent TFF1 gene in testicular tissue. Therefore, our data implicate, that in vivo exposure 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.
Permanent Link: http://hdl.handle.net/11104/0223161