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PM2.5 induces male reproductive toxicity via mitochondrial dysfunction, DNA damage and RIPK1 mediated apoptotic signaling pathway
Zhang, Jin1,2; Liu, Jianhui1,2; Ren, Lihua1,3; Wei, Jialiu1,2; Duan, Junchao1,2; Zhang, Lefeng2,4; Zhou, Xianqing1,2; Sun, Zhiwei1,2
通讯作者Zhang, Lefeng(2,4) ; Zhou, Xianqing(1,2)
关键词PM2.5 DNA damage Apoptosis RIPK1 Mitochondrial damage Male reproductive toxicity
刊名SCIENCE OF THE TOTAL ENVIRONMENT
2018-09-01
DOI10.1016/j.scitotenv.2018.03.383
634页:1435-1444
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Environmental Sciences
研究领域[WOS]Environmental Sciences & Ecology
关键词[WOS]FINE PARTICULATE MATTER ; LOS-ANGELES BASIN ; CELL-CYCLE ARREST ; AIR-POLLUTION ; EPITHELIAL-CELLS ; EXPOSURE ; HEALTH ; URBAN ; DEATH ; GENERATION
英文摘要

Recent years, air pollution has been a serious problem, and PM2.5 is the main air particulate pollutant. Studies have investigated that PM2.5 is a risky factor to the deterioration of semen quality inmales. But, the related mechanismis still unclear. To explore the effect of PM2.5, Sprague Dawley (SD) rats were exposed to PM2.5 (0, 1.8, 5.4 and 16.2 mg/kg.bw.) through intratracheal instillation. The exposure was performed once every 3 days and continued for 30 days. In vitro, GC-2spd cells were treated using 0, 50, 100, 200 mu g/mL PM2.5 for 24 h. The data showed that sperm relative motility rates and density were remarkably decreased, while sperm malformation rates were significantly increased with exposure to the PM2.5. The expression of Fas/FasL/RIPK1/FADD/Caspase-8/Caspase-3 and the level of 8-OHdG expression in testes were significantly increased after exposure to PM2.5. Additionally, in vitro the results showed that PM2.5 inhibited cell viability, increased the release of lactate dehydrogenase (LDH) by increasing reactive oxygen species (ROS) level. And ROS induced-DNA damage led to cell cycle arrest at G0/G1 phases and proliferation inhibition. Similar to the vivo study, the expressions of Fas/FasL/RIPK1/FADD/Caspase-8/Caspase-3 in GC-2spd cells were significantly increased after exposure to PM2.5 for 24-h. In addition, PM2.5 decreased the levels of ATP by impairing mitochondria structures, which led to energy metabolism obstruction resulted in the decrease of sperm motility. The above three aspects together resulted in the decrease in sperm quantity and quality. (C) 2018 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000433153600147
通讯作者邮箱lefengzhang163@163.com ; xqzhou2@163.com
第一作者单位Capital Med Univ, Sch Publ Hlth, Dept Toxicol & Hygien Chem, Beijing 100069, Peoples R China ; Capital Med Univ, Beijing Key Lab Environm Toxicol, Beijing 100069, Peoples R China
通讯作者单位Capital Med Univ, Sch Publ Hlth, Dept Toxicol & Hygien Chem, Beijing 100069, Peoples R China ; Capital Med Univ, Beijing Key Lab Environm Toxicol, Beijing 100069, Peoples R China ; Capital Med Univ, Sch Publ Hlth, Dept Occupat Hlth & Environm Hlth, Beijing 100069, Peoples R China
ISSN0048-9697
引用统计
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/141970
专题北京大学护理学院
北京大学口腔医学院_材料检测中心
作者单位1.Peking Univ, Sch Nursing, Beijing 100191, Peoples R China;
2.Capital Med Univ, Sch Publ Hlth, Dept Toxicol & Hygien Chem, Beijing 100069, Peoples R China;
3.Capital Med Univ, Beijing Key Lab Environm Toxicol, Beijing 100069, Peoples R China;
4.Capital Med Univ, Sch Publ Hlth, Dept Occupat Hlth & Environm Hlth, Beijing 100069, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Jin,Liu, Jianhui,Ren, Lihua,et al. PM2.5 induces male reproductive toxicity via mitochondrial dysfunction, DNA damage and RIPK1 mediated apoptotic signaling pathway[J]. SCIENCE OF THE TOTAL ENVIRONMENT,2018,634:1435-1444.
APA Zhang, Jin.,Liu, Jianhui.,Ren, Lihua.,Wei, Jialiu.,Duan, Junchao.,...&Sun, Zhiwei.(2018).PM2.5 induces male reproductive toxicity via mitochondrial dysfunction, DNA damage and RIPK1 mediated apoptotic signaling pathway.SCIENCE OF THE TOTAL ENVIRONMENT,634,1435-1444.
MLA Zhang, Jin,et al."PM2.5 induces male reproductive toxicity via mitochondrial dysfunction, DNA damage and RIPK1 mediated apoptotic signaling pathway".SCIENCE OF THE TOTAL ENVIRONMENT 634(2018):1435-1444.
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