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
中科院分区:
文献类型:
--
作者:
Yin Jiechen;Jian Zihai;Zhu Guangcan;Yu Xiaojin;Pu Yuepu;Yin Lihong;Wang Dayong;Bu Yuanqing;Liu Ran
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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影响因子:
6.9
作者:
Wang Yuxin;Zhong Yuxin;Li Jingguang;Zhang Jianqing;Lyu Bing;Zhao Yunfeng;Wu Yongning
通讯作者:
Wu Yongning
DOI:
10.1534/g3.114.012385
发表时间:
2014-08-12
期刊:
G3 (Bethesda, Md.)
影响因子:
--
作者:
Shinya R;Hasegawa K;Chen A;Kanzaki N;Sternberg PW
通讯作者:
Sternberg PW
影响因子:
7.3
作者:
Ellis RE;Stanfield GM
通讯作者:
Stanfield GM
DOI:
10.1016/j.reprotox.2011.05.024
发表时间:
2012-07
期刊:
Reproductive toxicology (Elmsford, N.Y.)
影响因子:
--
作者:
Raymer JH;Michael LC;Studabaker WB;Olsen GW;Sloan CS;Wilcosky T;Walmer DK
通讯作者:
Walmer DK
影响因子:
6.8
作者:
Jiechen Yin;Ran Liu;Zihai Jian;Dong Yang;Yuepu Pu;L. Yin;Dayong Wang
通讯作者:
Jiechen Yin;Ran Liu;Zihai Jian;Dong Yang;Yuepu Pu;L. Yin;Dayong Wang