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首页> 外文期刊>Reproductive toxicology >17α-Ethinylestradiol and nonylphenol affect the development of forebrain GnRH neurons through an estrogen receptors-dependent pathway
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17α-Ethinylestradiol and nonylphenol affect the development of forebrain GnRH neurons through an estrogen receptors-dependent pathway

机译：17α-乙炔雌二醇和壬基酚通过雌激素受体依赖性途径影响前脑GnRH神经元的发育

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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 17α-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.
机译：越来越多的证据表明，EDC靶向控制发育和繁殖的神经内分泌回路。我们以前已经证明，低浓度的17α-炔雌醇（EE2）会在斑马鱼发育过程中破坏前脑GnRH神经元的发育。本研究的目的是确定弱雌激素化合物壬基酚（NP）是否可以引起与EE2类似的作用，以及雌激素受体介导这些作用的程度。使用免疫组织化学，我们证实了EE2暴露诱导了GnRH-ir神经元数量的增加，并且我们证明了NP能够以浓度依赖性的方式产生类似的作用。 NP和EE2的作用均被雌激素受体拮抗剂ICI 182-780阻断，表明功能性ER参与介导其作用。这些结果共同凸显了将神经内分泌网络视为关键终点的必要性。在内分泌干扰领域。

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