Laboratory of Reproductive Biology, Institute of Biotechnology, Academy of Sciences of the Czech Republic, v. v. i., Videnska 1083, 142 20 Prague, Czech Republic.
Reproduction. 2013 Mar 7;145(3):255-63. doi: 10.1530/REP-12-0472. Print 2013 Mar 1.
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.
雌激素在精子发生中起着至关重要的作用，雌激素受体α敲除的雄性小鼠不育。已经证明，雌激素可显著增加体外获能的速度；然而，这可能会由于这些精子进行顶体反应的能力下降而降低生殖潜力。迄今为止，雌激素对精子获能能力的体内影响尚未被研究过。因此，在这项研究中，我们用 20ng/ml 的 17β-雌二醇（E2）处理小鼠（n=24），一种处理方式是在青春期（从第 4 周到第 7 周），另一种是从出生开始连续处理 12 周（n=8），这两种处理方式的动物都在 12 周时处死。通过酪氨酸磷酸化（TyrP）抗体（免疫荧光和 Western blot）和氯化四环素（CTC）检测分析附睾和睾丸精子的获能状态。根据我们的结果，体内暴露于增加的 E2 浓度会导致附睾精子过早获能。然而，E2 的作用似乎是可逆的，因为在青春期处理动物的暴露结束后，提前获能的附睾精子数量减少。此外，通过 TyrP 和 CTC 检测到的附睾精子获能状态的变化与血浆中 E2 水平和睾丸组织中雌激素依赖性三叶因子 1（Tff1）基因的表达呈正相关。因此，我们的数据表明，在特定条件下体内暴露于 E2 会导致小鼠附睾精子过早获能，这可能对精子在雌性生殖道中的生殖适应性产生负面影响。
