In vivo expusure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F13%3A00462938" target="_blank" >RIV/86652036:_____/13:00462938 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1530/REP-12-0472" target="_blank" >http://dx.doi.org/10.1530/REP-12-0472</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1530/REP-12-0472" target="_blank" >10.1530/REP-12-0472</a>

Result language

angličtina

Original language name

In vivo expusure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Original language description

Estrogens play a crucial role in spermatogenesis and estrogen receptor α 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. To date 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 17β-estradiol (E2) at the concentration of 20 ng/ml either during puberty from the fourth to seventh 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 killed. The capacitation status of epididymal and testicular sperm was analysed by tyrosine phosphorylation (TyrP) antibody (immunofluorescence and western blot) and chlortetracycline (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 animals treated during puberty. 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 trefoil factor 1 (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.

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

CE - Biochemistry

OECD FORD branch

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Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

Z - Vyzkumny zamer (s odkazem do CEZ)

Publication year

2013

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Reproduction

ISSN

1470-1626

e-ISSN

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Volume of the periodical

145

Issue of the periodical within the volume

March 2013

Country of publishing house

GB - UNITED KINGDOM

Number of pages

9

Pages from-to

255-263

UT code for WoS article

000317562900007

EID of the result in the Scopus database

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