title: In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis.
abstract: 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.
authors: Laboratory of Reproductive Biology, Institute of Biotechnology, Academy of Sciences of the Czech Republic, v. v. i., Videnska 1083, 142 20 Prague, Czech Republic. lukas.ded@img.cas.cz
authors: Lukas
authors: L
authors: Ded
authors: Natasa
authors: N
authors: Sebkova
authors: Martina
authors: M
authors: Cerna
authors: Fatima
authors: F
authors: Elzeinova
authors: Pavla
authors: P
authors: Dostalova
authors: Jana
authors: J
authors: Peknicova
authors: Katerina
authors: K
authors: Dvorakova-Hortova
mesh_terms: D000367:Age Factors; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D002751:Chlortetracycline / Q000378:metabolism; D004334:Drug Administration Schedule; D004822:Epididymis / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004958:Estradiol / Q000008:administration & dosage* / Q000097:blood; D005455:Fluorescent Antibody Technique; D008297:Male; D051379:Mice; D010455:Peptides / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D046468:Sexual Development; D013075:Sperm Capacitation / Q000187:drug effects*; D013094:Spermatozoa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013737:Testis / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D000071163:Trefoil Factor-1; D014443:Tyrosine
chemical_list: D015415:Biomarkers; D010455:Peptides; C472724:Tff1 protein, mouse; D000071163:Trefoil Factor-1; D014443:Tyrosine; D004958:Estradiol; D002751:Chlortetracycline