17α-Ethinylestradiol induces an imbalance between apoptosis and cell proliferation to sex steroid disruption in a testis culture of gudgeon, Gobio Gobio

S. Nadzialek, P. Kestemont

Résultats de recherche: Contribution à un journal/une revueArticle

Résumé

The aim of this study was to investigate the effect of the most potent xenoestrogen currently found in the environment, ethinylestradiol (EE2), on some physiological events occurring during early spermatogenesis of gudgeon (Gobio gobio), a common European fish species. Physiological pathways studies were apoptosis, cell proliferation, and steroidogenesis on sex steroids (testosterone [T], 11-ketotestosterone [11-KT], and 17β-estradiol [E2]). Testis pieces were cultured in vitro during 21 d at 10, 10, 10 , 10, 1 and 10 μg/L of EE2 as well as in positive (10 μg/L of E2) and ethanol control medium. Apoptosis and cell proliferation displayed opposite responses related to the EE2 concentration. When apoptosis inhibition was observed, cell proliferation was induced at 10 and 10 μg/L of EE2 as well as in the positive control. In contrast, a massive cell death was detected for high EE2 concentrations (1 and 10 μg/L). Steroidogenesis was also disrupted in a dose-related manner. 11-Ketotestosterone was depressed at 10 and 10 μg/L of EE2 whereas E2 was detectable in the medium only at 10, 10, and 10 μg/L of EE2. High concentrations of T were detected in the medium at 10, 10 , and 10 μg/L of EE2 but depressed at 1 and 10 μg/L of EE2. In conclusion, intermediate EE2 concentrations (10 and 10 μg/L) used in this experimental design have obviously disrupted early spermatogenesis, leading to an imbalance between cell death and cell proliferation in a sex steroid environment toward E2. The results of the present study could be the basis conditions for oocyte development within the testis of a common teleost fish under xenoestrogen exposure.
langue originaleAnglais
Pages (de - à)881-886
Nombre de pages6
journalEnvironmental Toxicology and Chemistry
Volume29
Numéro de publication4
Les DOIs
étatPublié - 1 janv. 2010

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