...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of applied toxicology >Diethylstilbestrol impaired oogenesis of yellow catfish juveniles through disrupting hypothalamic-pituitary-gonadal axis and germ cell development
【24h】

Diethylstilbestrol impaired oogenesis of yellow catfish juveniles through disrupting hypothalamic-pituitary-gonadal axis and germ cell development

机译：通过破坏下丘脑 - 垂体 - 性腺轴和生殖细胞发育，二乙基斯特洛尔患黄鲶青少年的卵泡作用受损

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Abstract Diethylstilbestrol (DES), a non-steroidal estrogen, has been found to cause altered germ cell development and disordered ovarian development in fish females. However, the mechanisms that might be involved are poorly understood. In this study, female juveniles of yellow catfish (Pelteobagrus fulvidraco) (120 days post-hatching) were exposed to two doses (10 and 100 ng /~(-1)) of DES for 28 days. After the endpoint of exposure, decreased ovary weight and gonadosomatic index, as well as various ovarian impairments were observed in response to DES. Besides, DES elevated the mRNA levels of vitellogenin 1 (vtg 1) and estrogen receptor 1 (esr 1) in liver and decreased 17beta-estradiol level in plasma. Correspondingly, suppressed mRNA levels of the key genes in the hypothalamic-pituitary-gonadal axis (such as cypl9a1b, gnrh-ll, fshfl and /hbeta in brain and fshr, Ihr and cypl9a1a in ovary) after DES exposure were also observed. The declined level of plasma 17beta-estradiol and altered gene expressions of genes in the hypothalamic-pituitary-gonadal axis were thus supposed to be closely related to the disrupted oogenesis in DES-treated fish. Analyses further demonstrated that, higher concentration of DES elevated the expression ratio of bax/bcl-2, indicating the enhanced apoptosis occurred in ovary. Moreover, DES upregulated the expressions of genes involved in proliferation (cyclin d1 and pcna), meiotic entry {cyp26al and scp3) and meiotic maintenance (dmc1), resulting in arrested oogenesis in catfish. The present study greatly extended our understanding on the mechanisms underlying of reproductive toxicity of DES on fish oogenesis.
机译：摘要已发现非甾体雌激素（DES），非甾体雌激素，导致鱼女性中的胚芽细胞发育和卵巢发育紊乱。然而，可能涉及的机制被理解得很差。在这项研究中，黄鲶（Pelteobagrus Fulvidraco）（孵化后120天）的雌性幼年暴露于DES 28天的两剂（10和100ng /〜（-1））。在暴露的终点后，卵巢重量和促性腺指数下降，以及响应于DES，观察到各种卵巢损伤。此外，DES在肝脏中升高了vallogenin1（Vtg 1）和雌激素受体1（ESR1）的mRNA水平，并降低了血浆中的17beta-雌二醇水平。还观察到，在DES暴露后，相应地，抑制了下丘脑 - 垂体 - 性腺轴颈中的关键基因的密钥基因的mRNA水平（例如Cypl9a1b，gnrh-ll，fshfl和/ hbeta，卵巢中的卵巢中的卵巢，Ihr和cypl9a1a）。因此，下丘脑 - 垂体性腺轴线中基因的血浆17beta-雌二醇和改变基因表达的下降水平应该与DES处理的鱼中断的血液发生密切相关。进一步证明，更高浓度的DES升高了Bax / Bcl-2的表达比，表明在卵巢中发生增强的凋亡。此外，DES上调了参与增殖（细胞周期蛋白D1和PCNA），减数分裂{CYP26和SCP3）和减数分裂（DMC1）的基因表达，导致鲶鱼中的oferoisesis。本研究大大扩大了我们对鱼类卵泡生殖毒性潜在的机制的理解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号