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In vivo exposure to 17B-estradiol triggers premature sperm capacitation in cauda epididymis
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SYSNO ASEP 0394635 Document Type A - Abstract R&D Document Type The record was not marked in the RIV R&D Document Type Není vybrán druh dokumentu Title In vivo exposure to 17B-estradiol triggers premature sperm capacitation in cauda epididymis Author(s) Děd, Lukáš (BTO-N) RID
Šebková, N. (CZ)
Černá, M. (CZ)
Elzeinová, Fatima (BTO-N) RID
Dostálová, Pavla (BTO-N)
Pěknicová, Jana (BTO-N) RID
Dvořáková-Hortová, K. (CZ)Number of authors 7 Source Title Book of abstracts. - Praha : Biotechnologický ústav, 2013 / Pěknicová Jana ; Kubátová Alena ; Elzeinová Fatima
S. 20-21Number of pages 2 s. Publication form Print - P Action XIX. Symposium imunologie a biologie reprodukce s mezinárodní účastí Event date 23.05.2013-25.05.2013 VEvent location Třešť Country CZ - Czech Republic Event type WRD Language eng - English Country CZ - Czech Republic Keywords Estrogen ; Sperm capacitation ; 17β-estradiol Subject RIV DN - Health Impact of the Environment Quality R&D Projects GA523/09/1793 GA ČR - Czech Science Foundation (CSF) CEZ AV0Z50520701 - BTO-N (2007-2013) Annotation 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. Workplace Institute of Biotechnology Contact Monika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700 Year of Publishing 2014
Number of the records: 1