Human Reproduction, Vol. 18, No. 1, 100-107,
January 2003
© 2003 European Society of Human Reproduction and Embryology
17ß-Estradiol and environmental estrogens significantly affect mammalian sperm function*
Centre for Reproduction, Endocrinology and Diabetes, School of Biomedical Sciences, Kings College London, London, UK 1 To whom correspondence should be addressed at: Centre for Reproduction, Endocrinology and Diabetes, School of Biomedical Sciences, Kings College London, Guys Campus, London Bridge, London SE1 1UL, UK. e-mail: lynn.fraser{at}kcl.ac.uk
*Presented in part at the 18th Annual Meeting of the European Society of Human Reproduction and Embryology 2002, Vienna, Austria
BACKGROUND: Compounds with estrogenic activity can affect reproductive function in mammals. This study investigated possible effects of 17ß-estradiol (E2) and three weakly estrogenic environmental estrogens on mammalian sperm capacitation and fertilizing ability in vitro. METHODS: Uncapacitated and capacitated mouse sperm suspensions were incubated for 30 min in the presence of E2, genistein (Gen), 8-prenylnaringenin (8-PN) and nonylphenol (NP), and then assessed using chlortetracycline (CTC) fluorescence analysis. In addition, treated uncapacitated sperm suspensions were tested for changes in fertilizing ability. RESULTS: In uncapacitated cells, E2 at
1 µmol/l and Gen, 8-PN and NP at
0.001 µmol/l, significantly stimulated capacitation and acrosome reactions. Hydroxytamoxifen (an estrogen antagonist) did not inhibit responses to any of these compounds. In capacitated cells, E2 had no effect, but the other three compounds significantly stimulated acrosome reactions. Added to uncapacitated suspensions, 10 µmol/l E2, 0.1 µmol/l Gen and 0.1 µmol/l 8-PN all significantly stimulated sperm fertilizing ability (
76% oocytes fertilized) compared with untreated control sperm (
36%). CONCLUSIONS: This study provides the first evidence that E2 and environmental estrogens can significantly stimulate mammalian sperm capacitation, acrosome reactions and fertilizing ability, with the environmental estrogens being much more potent than E2. The inability of hydroxytamoxifen to block these responses suggests that classical estrogen receptors may not be involved. Whether these responses have effects on fertility in vivo remains to be determined, along with the mechanisms of action involved.
Key words: capacitation/fertilizing ability/genistein/nonylphenol/8-prenylnaringenin
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