Perfluorooctane sulfonate exposure causes gonadal developmental toxicity in Caenorhabditis elegans through ROS-induced DNA damage
Perfluorooctane sulfonate exposure causes gonadal developmental toxicity in Caenorhabditis elegans through ROS-induced DNA damage
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全氟辛烷磺酸暴露通过 ROS 诱导的 DNA 损伤导致秀丽隐杆线虫性腺发育毒性
DOI：
10.1016/j.chemosphere.2016.04.046
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发表时间：
2016-07-01
期刊：
影响因子：
8.8
通讯作者：
Wu, Lijun
中科院分区：
文献类型：
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作者：
Guo, Xiaoying;Li, Qingqing;Wu, Lijun
全氟辛烷磺酸（PFOS）是一种常见的持久性有机污染物，据报道，在许多动物研究中显示出潜在的发育毒性。然而，人们对它对生殖组织，特别是生殖细胞系的影响知之甚少。在本研究中，秀丽隐杆线虫作为体内实验模型，研究全氟辛烷磺酸暴露引起的发育毒性，特别是在性腺。我们的研究结果表明，全氟辛烷磺酸暴露显著延缓了性腺发育，如孵化的L1期幼虫暴露于全氟辛烷磺酸72小时后仍处于幼虫期的蠕虫数量增加所示。对接触全氟辛烷磺酸后生殖细胞增殖的调查表明，当L1期幼虫接触0-25.0 μ M全氟辛烷磺酸时，生殖细胞总数以剂量依赖方式减少。全氟辛烷磺酸暴露可诱导生殖细胞系中有丝分裂细胞周期短暂停滞和细胞凋亡。对生殖细胞增殖过程中的DNA损伤和活性氧的产生进行的定量分析表明，在全氟辛烷磺酸处理组中，HUS-1：GFP和活性氧的明显病灶显著增加，而在加入二甲基亚砜和甘露醇后，全氟辛烷磺酸暴露引起的有丝分裂生殖细胞数量减少和细胞凋亡增加得到了有效挽救。这些结果表明，ROS诱导的DNA损伤可能在性腺发育的损害中起着关键作用，所示的总生殖细胞减少，短暂的有丝分裂细胞周期阻滞和细胞凋亡。(C)2016爱思唯尔有限公司版权所有
Perfluorooctane sulfonate (PFOS), a common persistent organic pollutant, has been reported to show potential developmental toxicity in many animal studies. However, little was known about its effects on reproductive tissues, especially in the germ line. In the present study, Caenorhabditis elegans was used as an in vivo experimental model to study the developmental toxicity caused by PFOS exposure, especially in the gonads. Our results showed that PFOS exposure significantly retarded gonadal development, as shown by the increased number of worms that remained in the larval stages after hatched L1-stage larvae were exposed to PFOS for 72 h. Investigation of germ line proliferation following PFOS exposure showed that the number of total germ cells reduced in a dose-dependent manner when L1-stage larvae were exposed to 0-25.0 mu M PFOS. PFOS exposure induced transient mitotic cell cycle arrest and apoptosis in the germ line. Quantification of DNA damage in proliferating germ cells and production of reactive oxygen species (ROS) showed that distinct foci of HUS-1:GFP and ROS significantly increased in the PFOS-treated groups, whereas the decrease in mitotic germ cell number and the enhanced apoptosis induced by PFOS exposure were effectively rescued upon addition of dimethyl sulfoxide (DMSO) and mannitol (MNT). These results suggested that ROS-induced DNA damage might play a pivotal role in the impairment of gonadal development indicated by the reduction in total germ cells, transient mitotic cell cycle arrest, and apoptosis. (C) 2016 Elsevier Ltd. All rights reserved.