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]Department of Urology, Tong Ren Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
Polybrominated diphenyl ethers may affect male reproductive function; however, the underlying mechanism is still uncertain. By using Caenorhabditis elegans, a commonly used model to study basic biological processes in apoptosis, we investigated the toxic effects of 4-bromodiphenyl ether (BDE-3), the most fundamental mono-BDE generated from degradation of polybrominated diphenyl ethers in the environment. We found that BDE-3 treated worms exhibited decreased life spans, impaired fecundity and delayed egg laying. BDE-3 induced dose-dependent germ cell apoptosis in wild-type N2 strain; however, this effect was blocked in mutants of p53/cep-1 and DNA damage response gene hus-1. Moreover, the knockout of the MAPK kinases (mutants mek-1 and sek-1) and the p53 antagonist protein ABL-1 (abl-1), which are essential for stress-induced germ cell apoptosis, also abrogated the germ cell apoptosis induced by BDE-3. Generation of reactive oxygen species (ROS) in intact animals was determined by a fluorescent probe, 2,7-dichlorofluorescein diacetate, and the ROS level was significantly elevated by BDE-3 treatment. Microarray analysis on gene expression profiles further revealed the possible pathways involved in BDE-3 toxicity. Overall, our findings suggested that BDE-3 could induce reproductive dysfunction and germ cell apoptosis in C. elegans by induction of ROS and DNA damage.
基金：
The work herein was supported by grants from the 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：
通讯机构：[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]Department of Urology, Tong Ren Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China[*1]Hongqiao International Institute of Medicine, Shanghai Tong Ren Hospital and Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, 227 South Chongqing Road, Shanghai 200025, China.[*2]Tong Ren Hospital Affiliated To Shanghai Jiao Tong University School Of Medicine, 1111 Xianxia Road, Shanghai 200336, China.
推荐引用方式(GB/T 7714)：
You Xinyue,Xi Jing,Cao Yiyi,et al.4-Bromodiphenyl Ether Induces Germ Cell Apoptosis by Induction of ROS and DNA Damage in Caenorhabditis elegans[J].TOXICOLOGICAL SCIENCES.2017,157(2):510-518.doi:10.1093/toxsci/kfx064.
APA：
You, Xinyue,Xi, Jing,Cao, Yiyi,Zhang, Jinfu&Luan, Yang.(2017).4-Bromodiphenyl Ether Induces Germ Cell Apoptosis by Induction of ROS and DNA Damage in Caenorhabditis elegans.TOXICOLOGICAL SCIENCES,157,(2)
MLA：
You, Xinyue,et al."4-Bromodiphenyl Ether Induces Germ Cell Apoptosis by Induction of ROS and DNA Damage in Caenorhabditis elegans".TOXICOLOGICAL SCIENCES 157..2(2017):510-518
