17伪-Ethinylestradiol and nonylphenol affect the development of forebrain GnRH neurons through an estrogen receptors-dependent pathway

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• 作者：Mé ; lanie Vosges^a ; Olivier Kah^b ; Nathalie Hinfray^a ; Edith Chadili^a ; Yann Le Page^b ; Yves Combarnous^c ; Jean-Marc Porcher^a ; Franç ; ois Brion^a ; ^{francois.brion@ineris.fr}
• 关键词：AroB ; aromatase B ; dpf ; days post-fertilization ; EDC ; endocrine disrupting chemical ; ER ; estrogen receptor ; EE2 ; ethinylestradiol ; GnRH ; gonadotropin-releasing hormone ; ir ; immunoreactive ; NP ; nonylphenol
• 刊名：Reproductive Toxicology
• 出版年：2012
• 期刊代码：233_08906238
• 类别：med
• 出版时间：April, 2012
• 卷：33
• 期：2
• 页码：198-204
• 文件大小：1041 K

摘要

There is growing evidence that neuroendocrine circuits controlling development and reproduction are targeted by EDCs. We have previously demonstrated that low concentrations of 17伪-ethinylestradiol (EE2) disrupt the development of forebrain GnRH neurons during zebrafish development. The objectives of the present study were to determine whether the weak estrogenic compound, nonylphenol (NP), could elicit similar effects to EE2 and to what extent the estrogen receptors are involved in mediating these effects. Using immunohistochemistry, we confirmed that EE2 exposure induces an increase in the number of GnRH-ir neurons and we demonstrated that NP is able to produce similar effects in a concentration-dependent manner. The effects of both NP and EE2 were shown to be blocked by the estrogen receptors (ERs) antagonist ICI 182-780, demonstrating the involvement of functional ERs in mediating their effects.

Altogether, these results highlight the need to consider neuroendocrine networks as critical endpoints in the field of endocrine disruption.