文献类型：期刊文献

英文题名：Chronic toxicity of hexabromocyclododecane(HBCD) induced by oxidative stress and cell apoptosis on nematode Caenorhabditis elegans

作者：Wang, Xiaoli[1];Yang, Jie[2];Li, Hui[1,3];Guo, Shu[4];Tariq, Muhammad[1];Chen, Haibo[4];Wang, Chen[1];Liu, Yongdi[1]

机构：[1]East China Univ Sci & Technol, Sch Resources & Environm Engn, State Environm Protect Key Lab Environm Risk Asse, Shanghai 200237, Peoples R China;[2]Shanghai Acad Environm Sci, Res Inst Wastes & Soil Remediat, Shanghai 200233, Peoples R China;[3]Shanghai Univ, Inst Environm Pollut & Hlth, Shanghai 201800, Peoples R China;[4]MEP, South China Inst Environm Sci, Ctr Environm Hlth Res, Guangzhou 510535, Guangdong, Peoples R China

年份：2018

卷号：208

起止页码：31

外文期刊名：CHEMOSPHERE

收录：;EI(收录号：20182705406860);WOS:【SCI-EXPANDED(收录号:WOS:000441999400004)】；

基金：This work was supported jointly by the National key research and development plan (2016YFC0206200), the National Natural Science Foundation of China (51578240), the Fok Ying Tung Education Foundation (141077), Open Foundation of State Key Laboratory of Environmental Criteria and Risk Assessment Chinese Research Academy of Environmental Sciences (SKLE-CRA2016OFP19), Program of Shanghai Academic/Technology Research Leader (18XD1424100), Open Foundation of Shanghai Key Lab for Urban Ecological Processes and Eco-Restoration, and the Innovation Program of the Shanghai Municipal Education Commission (14ZZ059). 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; Chronic exposure; Oxidative stress; Cell apoptosis

摘要：In order to gain insights into the chronic effects and mechanisms of hexabromocyclododecane (HBCD), the animal model Caenorhabditis elegans (C. elegans) was chosen for toxicity study. Multiple endpoints, including the physiological (growth and locomotion behaviors), biochemical (reactive oxygen species (ROS) production, lipofuscin accumulation, and cell apoptosis), and molecular (stress-related gene expressions) levels, were tested by chronic exposure for 10 d to low concentrations of HBCD (0.2 nM 200 nM). The results revealed that chronic exposure to HBCD at concentrations more than 20 nM would significantly influence the growth, locomotion behaviors, ROS formation, lipofuscin accumulation, and cell apoptosis of nematodes. Treatment with antioxidants of ascorbate and N-acetyl-(L)-cysteine (NAC) suppressed the toxicity induced by HBCD. The integrated gene expression profiles showed that the chronic exposure to 200 nM of HBCD significantly increased the expression levels of stress-related genes (e.g., hsp-16.2, hsp-16.48, sod-1, sod-3, and cep-1 genes). Among these genes, the sod-1, sod-3, and cep-1 gene expressions were significantly correlated with HBCD-induced physiological effects by the Pearson correlation test. The mutations of sod-3 and cep-1 induced more severe toxicity compared to wild-type nematodes. Therefore, HBCD exposure induced oxidative stress by ROS accumulation and cell apoptosis,which resulted in HBCD-induced toxicity on nematodes, and sod-3 and cep-1 played important roles in protecting nematodes against HBCD-induced toxicity. (C) 2018 Elsevier Ltd. All rights reserved.