Male reproductive toxicity involved in spermatogenesis induced by perfluorooctane sulfonate and perfluorooctanoic acid in Caenorhabditis elegans

Male reproductive toxicity involved in spermatogenesis induced by perfluorooctane sulfonate and perfluorooctanoic acid in Caenorhabditis elegans
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全氟辛烷磺酸和全氟辛酸诱导秀丽隐杆线虫精子发生的雄性生殖毒性

DOI:
10.1007/s11356-020-10530-8
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发表时间:
2020-08
影响因子:
5.8
通讯作者:
Liu Ran
Liu Ran
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Yin Jiechen;Jian Zihai;Zhu Guangcan;Yu Xiaojin;Pu Yuepu;Yin Lihong;Wang Dayong;Bu Yuanqing;Liu Ran

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全氟辛烷磺酸(PFOS)和全氟辛酸(PFOA)作为一种持久性有机污染物,由于其对人类和环境的潜在危害,近年来受到越来越多的研究关注。本文采用活性炭法研究了这些污染物的生殖毒性。elegans模型,通过暴露于0.001、0.01和0.1 mmol/L全氟辛烷磺酸或全氟辛酸48小时,评估him-5小鼠整个发育周期的精子发生情况。实验结果表明,接触全氟辛烷磺酸和全氟辛酸会导致幼仔数量、生殖细胞数量、精子细胞大小和活力减少,精子细胞畸形率增加。方差分析(ANOVA)显示,仅在0.001 mmol/L暴露组中,PFOS暴露导致生殖细胞损伤水平高于PFOA。RT-qPCR用于进一步研究与精子发生的不同阶段相关的基因的表达,例如有丝分裂和减数分裂、纤维体膜细胞器(FB-MO)和精子活化。wee-1.3、spe-4、spe-6和spe-17基因表达水平升高,而puf-8、spe-10、fer-1、swm-1、try-5和spe-15基因表达水平降低。我们的研究结果表明,PFOS或PFOA可能会通过破坏有丝分裂增殖、减数分裂进入、MO的形成、MO与质膜(PM)的融合以及伪足而导致精子发生损伤。利用puf-8和spe-10突变体进行的功能丧失研究表明,spe-10基因通过调控一个或多个关键的棕榈酰化事件特异性参与PFOS或PFOA诱导的生殖毒性,而puf-8基因不是PFOS和PFOA的直接靶基因,PFOS和PFOA可能作用于puf-8的上游基因,从而影响生殖能力。综上所述,这些结果证明了全氟辛烷磺酸和全氟辛酸对精子发生的潜在不利影响,并为全氟辛烷磺酸风险评估提供了宝贵的数据。
As a persistent organic pollutant, perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) have gained increasing research attention over recent years because of their potential risk to humans and the environment. In this paper, we investigated the reproductive toxicity of these pollutants using aC. elegansmodel to evaluate spermatogenesis throughout the entire developmental cycle ofhim-5 mutantby exposing to 0.001, 0.01, and 0.1 mmol/L PFOS or PFOA for 48 h. Experimental results suggested that PFOS and PFOA exposure led to reductions in brood size, germ cell number, spermatid size, and motility, and increases in rate of malformation spermatids. Analysis of variance (ANOVA) showed that exposure to PFOS resulted in higher levels of damage than PFOA in germ cells only in 0.001 mmol/L exposure group. RT-qPCR was used to further investigate the expression of genes associated with different stages of spermatogenesis, such as mitosis and meiosis, fibrous body-membranous organelles (FB-MOs), and sperm activation. The expression levels ofwee-1.3,spe-4,spe-6, andspe-17genes were increased, while those ofpuf-8,spe-10,fer-1,swm-1,try-5, andspe-15genes were decreased. Our results suggesting that PFOS or PFOA may cause spermatogenesis damage by disrupting the mitotic proliferation, meiotic entry, formation of the MOs, fusion of the MOs and plasma membrane (PM), and pseudopods. Loss-of-function studies usingpuf-8andspe-10mutants revealedspe-10gene was specifically involved in PFOS- or PFOA-induced reproductive toxicity via regulating one or more critical palmitoylation events, whilepuf-8gene was not direct target of PFOS and PFOA, and PFOS and PFOA may act on the upstream gene ofpuf-8, thus affecting reproductive ability. Taken together, these results demonstrate the potential adverse impact of PFOS and PFOA exposure on spermatogenesis and provide valuable data for PFC risk assessment.
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DOI: 10.1016/j.jes.2017.08.017
发表时间: 2018
影响因子: 6.9
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期刊: G3 (Bethesda, Md.)
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发表时间: 2012-07
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发表时间: 2018-11
影响因子: 6.8
作者:
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