文献类型：期刊文献

中文题名：六溴环十二烷急性暴露对秀丽隐杆线虫的毒性效应

英文题名：Toxicological Effects of Hexabromocyclododecane (HBCD) by Acute Exposure on Nematode Caenorhabditis Elegans

作者：陈海波[1];李辉[1];刘勇弟[1]

机构：[1]华东理工大学资源与环境工程学院,上海200237

年份：2019

卷号：45

期号：1

起止页码：87

中文期刊名：华东理工大学学报（自然科学版）

外文期刊名：Journal of East China University of Science and Technology

收录：CSTPCD;;Scopus;北大核心:【北大核心2017】；CSCD:【CSCD_E2019_2020】；

基金：国家重点研发计划(2016YFC0206200);中国环境科学研究院环境基准与风险评估国家重点实验室开放基金(SKLECRA2016OFP19);上海市城市化生态过程与生态恢复重点实验室开放基金

语种：中文

中文关键词：六溴环十二烷;秀丽隐杆线虫;氧化应激;细胞凋亡

外文关键词：hexabromocyclododecane;Caenorhabditis elegans;oxidative stress;cell apoptosis

摘要：以秀丽隐杆线虫作为模式生物,从生理(体长、运动行为、产卵率),生化(活性氧水平ROS、细胞凋亡水平)及分子(14种胁迫相关基因表达)水平研究六溴环十二烷(HBCD)急性暴露对秀丽隐杆线虫的毒性效应。结果表明,当HBCD急性暴露浓度为20 nmol/L时,只会显著降低秀丽隐杆线虫的运动行为,表明运动行为是最敏感的生理指标。当HBCD急性暴露浓度为200 nmol/L时,秀丽隐杆线虫体内ROS水平和细胞凋亡水平显著提高。当HBCD急性暴露浓度为20～200 nmol/L时,秀丽隐杆线虫体内胁迫相关基因表达量明显上调,主要是氧化应激和细胞凋亡相关基因(hsp-16.2,hsp-16.48,sod-1,sod-3和cep-1)的影响。因此,HBCD可能通过氧化应激和细胞凋亡的途径对线虫产生毒性作用,并且hsp-16.2,hsp-16.48,sod-1,sod-3和cep-1基因具有调控秀丽隐杆线虫的氧化应激和细胞凋亡的作用。
Hexabromocyclododecane(HBCD)is extensively used as an additive brominated flame retardants(BFRs).Due to widespread spectra use of HBCD,it has been found universally in various environmental media including water,sediments,soil,and even in human milk.Moreover,it has multiple toxic effects including developmental toxicity,neurotoxicity and reproductive toxicity.Currently,many toxicological studies of HBCD have been carried out on aquatic organisms and terrestrial species.However,the toxicity of HBCD on soil nematodes is largely unknown.In order to understand toxicological effects along with the changes of stress response by HBCD exposure,the animal model Caenorhabditis elegans was chosen for toxicity study.To fulfill the tasks,nematodes were exposed to various concentrations of HBCD(0,0.2,2,20,200 nmol/L)up to 24 h.Multiple endpoints along with the physiological levels(growth,reproduction,and locomotion behaviors),reactive oxygen species(ROS)production,degree of cell apoptosis and stress-related gene expressions,were tested on nematodes.Acute exposure to HBCD at different concentrations domain of 0.2~ 200 nmol/L did not obviously decrease the body bends and body length on nematodes.In contrast,acute exposure to HBCD at the concentration of 20 nmol/L significantly decreased the locomotion behaviors on nematodes,and the locomotion behaviors were most sensitive among the physiological endpoints.Acute exposure to HBCD at the concentration of 200 nmol/L could significantly increase the ROS production followed by the enhancement in degree of cell apoptosis on nematodes.The integrated gene expression profiles visually revealed that exposure to HBCD at the concentration of 200 nmol/L resulted in obvious change of stress-related gene expressions,and the increased expressions were pronounced in several genes related to oxidative stress and cell apoptotic,e.g.,hsp-16.2,hsp-16.48,sod-1,sod-3 and cep-1 gene.Therefore,it was speculated that HBCD exposure induced the oxidative stress and cell apoptosis,which resulted in the adverse physiological effects.The hsp-16.2,hsp-16.4,sod-1,sod-3 and cep-1 gene may play important roles in HBCD-induced toxicity,and the oxidative stress and cell apoptosis could be regulated by hsp-16.2,hsp-16.4,sod-1,sod-3 and cep-1 gene.The results are helpful for understanding the toxic effects of HBCD and evaluating the potential risk of HBCD.