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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Aneuploid Sperm Formation In Rainbow Trout Exposed To The Environmental Estrogen 17α-ethynylestradiol
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Aneuploid Sperm Formation In Rainbow Trout Exposed To The Environmental Estrogen 17α-ethynylestradiol

机译：环境雌激素17α-炔雌醇暴露于虹鳟鱼的非整倍体精子形成

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摘要

Environmental contaminants that mimic native estrogens (i.e., environmental estrogens) are known to significantly impact a wide range of vertebrate species and have been implicated as a source for increasing human male reproductive deficiencies and diseases. Despite the widespread occurrence of environmental estrogens and recognized detrimental effects on male vertebrate reproduction, no specific mechanism has been determined indicating how reduced fertility and/or fecundity is achieved. Previous studies show that male rainbow trout, Oncorhynchus mykiss, exposed to the environmental estrogen 17α-ethynylestradiol (EE2) before gamete formation and fertilization produce progeny with significantly reduced embryonic survival. To determine whether this observed decrease results from sperm chromosome alterations during spermatogenesis, male rainbow trout were exposed to 10 ng of EE2/I for 50 days. After exposure, semen was collected and sperm aneuploidy levels analyzed with two chromosome markers by fluorescent in situ hybridization. In vitro fertilizations were also conducted by using control and exposed sperm crossed to eggs from an unexposed female for offspring analysis. Evaluations for nucleolar organizer region number and karyotype were performed on developing embryos to determine whether sperm aneuploidy translated into embryonic aneuploidy. Results conclusively show increased aneuploid sperm formation due to EE2 exposure. Additionally, embryonic cells from propagated progeny of individuals possessing elevated sperm aneuploidy display high levels of embryonic aneuploidy. This study concludes that EE2 exposure in sexually developing male rainbow trout increases levels of aneuploid sperm, providing a mechanism for decreased embryonic survival and ultimately diminished reproductive success in EE2 exposed males.
机译：已知模仿天然雌激素的环境污染物（即环境雌激素）会显着影响广泛的脊椎动物种类，并且已被认为是导致人类男性生殖能力不足和疾病增加的来源。尽管环境雌激素的广泛发生和对雄性脊椎动物繁殖的公认有害影响，但尚未确定指示如何实现降低的生育力和/或繁殖力的具体机制。先前的研究表明，雄性虹鳟Oncorhynchus mykiss在配子形成和受精前暴露于环境雌激素17α-乙炔雌二醇（EE2）会产生后代，其胚胎存活期显着降低。为了确定这种观察到的减少是否是由于精子发生过程中精子染色体的改变而导致的，将雄性虹鳟鱼暴露于10 ng EE2 / I 50天。暴露后，收集精液并通过荧光原位杂交用两个染色体标记分析精子非整倍性水平。还通过使用对照进行受精，并将未接触雌性的裸露精子与卵杂交，以进行后代分析。对发育中的胚进行了核仁组织区数目和核型的评估，以确定精子非整倍性是否转化为胚胎非整倍性。结果最终显示由于EE2暴露，非整倍体精子形成增加。另外，来自具有高精子非整倍性的个体的繁殖后代的胚胎细胞表现出高水平的胚胎非整倍性。这项研究的结论是，在性发育中的雄性虹鳟鱼中暴露于EE2会增加非整倍体精子的水平，从而为降低胚胎存活率并最终降低暴露于EE2的雄性中的生殖成功提供了一种机制。

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