机构：[1]Hongqiao International Institute of Medicine, Shanghai Tong Ren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China[2]Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai, 200444, China[3]Guangzhou Key Laboratory of Environmental Catalysis and Pollution Control, School of Environmental Science and Engineering, Institute of Environmental Health and Pollution Control, Guangdong University of Technology, Guangdong, 510006, China
2,2',4,4'-Tetrabromodiphenyl ether (BDE-47), a representative congener of polybrominated diphenyl ethers in the environment, is known to have reproductive toxicity. However, the underlying mechanisms remain to be clarified, especially in in vivo systems. In the present study, we employed Caenorhabditis elegans to study the effects of BDE-47 on reproduction. Our results showed that BDE-47 impaired worm fecundity and induced germ cell apoptosis. To elucidate the mechanisms, DNA damage and oxidative stress induction were investigated by determining the numbers of foci formation in transgenic worms expressing HUS-1::GFP and the levels of reactive oxygen species, respectively. We found that BDE-47 induced oxidative stress but not DNA damage, and treatment with the antioxidant, N-acetyl-Lcysteine, completely abrogated BDE-47-induced germ cell apoptosis. In addition, the apoptosis was blocked in mutants carrying mek-1, sek-1 or abl-1 loss-of-function alleles, but not in the p53/cep-1 deficient worms, suggesting that the mitogen-activated protein kinase (MAPK) signaling cascade was essential for BDE-47-induced germ cell apoptosis and p53/cep-1 was not required. Moreover, the apoptosis in the strains deficient for DNA damage response was not suppressed under BDE-47 treatment. Overall, we demonstrated that BDE-47 could induce oxidative stress and subsequent germ cell apoptosis in Caenorhabditis elegans through a MAPK-mediated p53-independent pathway. (C) 2018 Elsevier Ltd. All rights reserved.
基金：
National Natural Science
Foundation of China [grant number 21477078].
第一作者机构：[1]Hongqiao International Institute of Medicine, Shanghai Tong Ren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China
通讯作者：
推荐引用方式(GB/T 7714)：
You Xinyue,Xi Jing,Liu Weiying,et al.2,2 ',4,4 '-tetrabromodiphenyl ether induces germ cell apoptosis through oxidative stress by a MAPK-mediated p53-independent pathway[J].ENVIRONMENTAL POLLUTION.2018,242:887-893.doi:10.1016/j.envpol.2018.07.056.
APA：
You, Xinyue,Xi, Jing,Liu, Weiying,Cao, Yiyi,Tang, Weifeng...&Luan, Yang.(2018).2,2 ',4,4 '-tetrabromodiphenyl ether induces germ cell apoptosis through oxidative stress by a MAPK-mediated p53-independent pathway.ENVIRONMENTAL POLLUTION,242,
MLA：
You, Xinyue,et al."2,2 ',4,4 '-tetrabromodiphenyl ether induces germ cell apoptosis through oxidative stress by a MAPK-mediated p53-independent pathway".ENVIRONMENTAL POLLUTION 242.(2018):887-893
环境科学与生态学