文献类型：期刊文献

英文题名：Multi-generational effects and variations of stress response by hexabromocyclododecane (HBCD) exposure in the nematode Caenorhabditis elegans

作者：Chen, Haibo[1];Guo, Shu[1];Li, Hui[2];Zhou, Dong[3];Cao, Xue[4];Wang, Chen[4];Liu, Yongdi[4];Xiang, Mingdeng[1];Li, Liangzhong[1];Yu, Yunjiang[1]

机构：[1]South China Inst Environm Sci, Minist Environm Protect, State Environm Protect Key Lab Environm Pollut Hl, Guangzhou 510655, Guangdong, Peoples R China;[2]Shanghai Univ, Sch Environm & Chem Engn, Inst Environm Pollut & Hlth, Shanghai 200444, Peoples R China;[3]Shanghai Acad Environm Sci, Res Inst Wastes & Soil Remediat, Shanghai 200233, Peoples R China;[4]East China Univ Sci & Technol, Sch Resources & Environm Engn, State Environm Protect Key Lab Environm Risk Asse, Shanghai 200237, Peoples R China

年份：2019

卷号：245

起止页码：216

外文期刊名：JOURNAL OF ENVIRONMENTAL MANAGEMENT

收录：;EI(收录号：20233414609371);WOS:【SCI-EXPANDED(收录号:WOS:000473380300024)】；

基金：This work was supported jointly by the National Key Research and Development Plan (2016YFCO206200), the National Natural Science Foundation of China (41877377), the Program of Shanghai Academic/Technology Research Leader (18XD1424100), and the Open Foundation of State Key Laboratory of Environmental Criteria and Risk Assessment Chinese Research Academy of Environmental Sciences (SKLECRA20160FP19). We also would like to thank the anonymous referees for their helpful comments on this paper.

语种：英文

外文关键词：Caenorhabditis elegans; Hexabromocyclododecane; Multi-generational effect; Oxidative stress; Cell apoptosis

摘要：In order to understand multi-generational effects and changes of stress response by hexabromocyclododecane (HBCD) exposure, the animal model Caenorhabditis elegans was chosen for toxicity study. Multiple endpoints, including the physiological levels (growth, reproduction, and locomotion behaviors), stress-related gene expressions, reactive oxygen species (ROS) production and degree of cell apoptosis, were evaluated on exposed nematodes and their progeny. Prolonged exposure to HBCD at concentrations of 2 nM-200 nM caused adverse physiological effects in the parental generation (F0), and these effects were also observed in the offspring under HBCD-free conditions (F1). HBCD-induced toxicities could be transferred from parent to offspring. The integrated gene expressions profiles showed that exposure to HBCD at concentrations of 20-200 nM resulted in obvious changes in stress-related gene expressions, which were more increased in F0 generation than in F1 generation. The increased expressions were pronounced in several genes related to oxidative stress and cell apoptosis, e.g., hsp-16.2, hsp-16.48, sod-1, sod-3 and cep-1 genes. Exposure to 200 nM of HBCD could significantly increase ROS production and degree of cell apoptosis in the F0 and F1 generations. Therefore, it was speculated that HBCD exposure induced oxidative stress and cell apoptosis, which resulted in the adverse physiological effects. This finding is helpful for understanding the multi-generational effects and evaluating the potential risk of HBCD.