Open AccessRegulation and disruption of hamster sperm hyperactivation by progesterone, 17β‐estradiol and diethylstilbestrol
Author(s) -
Fujinoki Masakatsu
Publication year - 2014
Publication title -
reproductive medicine and biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.005
H-Index - 22
eISSN - 1447-0578
pISSN - 1445-5781
DOI - 10.1007/s12522-013-0175-8
Subject(s) - hyperactivation , diethylstilbestrol , hamster , sperm , endocrinology , medicine , chemistry , biology , andrology , hormone
Purpose Hyperactivation of hamster sperm is dose‐dependently enhanced by progesterone (P) and 17β‐estradiol (E). In the first part of the present study, enhancement of hyperactivation in response to the concentrations of P and E was examined in detail and in the second part, it was examined whether enhancement of hyperactivation by P and E was disrupted by diethylstilbestrol (DES). Methods Hamster spermatozoa were hyperactivated by incubation in modified Tyrode's albumin lactate pyruvate medium with P, E and/or DES. After spermatozoa were recorded using a video‐microscope, observations were quantified by manually counting the numbers of total, motile and hyperactivated spermatozoa. Results Hyperactivation was enhanced in response to the concentrations of P and E. When spermatozoa were exposed to DES with E, moreover, DES significantly and strongly suppressed P‐enhanced hyperactivation by accelerating the effect of E, but DES itself only weakly suppressed P‐enhanced hyperactivation. Conclusions Enhancement of hyperactivation was regulated by the concentrations of P and E, suggesting that in vivo hamster spermatozoa are hyperactivated through “monitoring” these concentrations in the oviduct. DES in combination with E suppressed P‐enhanced hyperactivation, suggesting that DES significantly disrupts hyperactivation by acting as an accelerator of the effect of E.