17β‐Estradiol and environmental estrogens significantly affect mammalian sperm function

• Published in: Human reproduction (Oxford) 2003-01, Vol.18 (1), p.100-107
• Main Authors: Adeoya‐Osiguwa, S.A., Markoulaki, S., Pocock, V., Milligan, S.R., Fraser, L.R.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Key words: capacitation/fertilizing ability/genistein/nonylphenol/8‐prenylnaringenin; Mammalian male genital system; Morphology. Physiology; Vertebrates: reproduction
• ISSN: 0268-1161; 1460-2350
• DOI: 10.1093/humrep/deg037

BACKGROUND: Compounds with estrogenic activity can affect reproductive function in mammals. This study investigated possible effects of 17β‐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.