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Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos

文献类型:期刊论文

作者Deng, Jun1,2; Yu, Liqin1,2; Liu, Chunsheng1; Yu, Ke1; Shi, Xiongjie1; Yeung, Leo W. Y.3; Lam, Paul K. S.3; Wu, Rudolf S. S.3; Zhou, Bingsheng1
刊名AQUATIC TOXICOLOGY
出版日期2009-06-04
卷号93期号:1页码:29-36
ISSN号0166-445X
关键词HBCD Developmental toxicity Apoptosis Zebrafish embryo Gene expression
通讯作者Zhou, BS, Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Donghu S Rd 7, Wuhan 430072, Peoples R China
中文摘要Hexabromocyclododecane (HBCD) is widely used as a brominated flame retardant, and has been detected in the aquatic environment, wild animals, and humans. However, details of the environmental health risk of HBCD are not well known. In this study, zebrafish embryos were used to assess the developmental toxicity of the chemical. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to various concentrations of HBCD (0, 0.05, 0.1, 0.5, and 1.0 mg L-1) until 96 h. Exposure to 0.1, 0.5, and 1.0 mg L-1 HBCD significantly increased the malformation rate and reduced survival in the 0.5 and 1.0 mg L-1 HBCD exposure groups. Acridine orange (AO) staining showed that HBCD exposure resulted in cell apoptosis. Reactive oxygen species (ROS) was significantly induced at exposures of 0.1, 0.5, and 1.0 mg L-1 HBCD. To test the apoptotic pathway, several genes related to cell apoptosis, such as p53, Puma, Apaf-1, caspase-9, and caspase-3, were examined using real-time PCR. The expression patterns of these genes were up-regulated to some extent. Two anti-apoptotic genes, Mdm2 (antagonist of p53) and Bcl-2 (inhibitor of Bax), were down-regulated, and the activity of capspase-9 and caspase-3 was significantly increased. The overall results demonstrate that waterborne HBCD is able to produce oxidative stress and induce apoptosis through the involvement of caspases in zebrafish embryos. The results also indicate that zebrafish embryos can serve as a reliable model for the developmental toxicity of HBCD. (C) 2009 Elsevier B.V. All rights reserved.
英文摘要Hexabromocyclododecane (HBCD) is widely used as a brominated flame retardant, and has been detected in the aquatic environment, wild animals, and humans. However, details of the environmental health risk of HBCD are not well known. In this study, zebrafish embryos were used to assess the developmental toxicity of the chemical. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to various concentrations of HBCD (0, 0.05, 0.1, 0.5, and 1.0 mg L(-1)) until 96 h. Exposure to 0.1, 0.5, and 1.0 mg L(-1) HBCD significantly increased the malformation rate and reduced survival in the 0.5 and 1.0 mg L(-1) HBCD exposure groups. Acridine orange (AO) staining showed that HBCD exposure resulted in cell apoptosis. Reactive oxygen species (ROS) was significantly induced at exposures of 0.1, 0.5, and 1.0 mg L(-1) HBCD. To test the apoptotic pathway, several genes related to cell apoptosis, such as p53, Puma, Apaf-1, caspase-9, and caspase-3, were examined using real-time PCR. The expression patterns of these genes were up-regulated to some extent. Two anti-apoptotic genes, Mdm2 (antagonist of p53) and Bcl-2 (inhibitor of Bax), were down-regulated, and the activity of capspase-9 and caspase-3 was significantly increased. The overall results demonstrate that waterborne HBCD is able to produce oxidative stress and induce apoptosis through the involvement of caspases in zebrafish embryos. The results also indicate that zebrafish embryos can serve as a reliable model for the developmental toxicity of HBCD. (C) 2009 Elsevier B.V. All rights reserved.
学科主题Marine & Freshwater Biology; Toxicology
WOS标题词Science & Technology ; Life Sciences & Biomedicine
类目[WOS]Marine & Freshwater Biology ; Toxicology
研究领域[WOS]Marine & Freshwater Biology ; Toxicology
关键词[WOS]BROMINATED FLAME RETARDANTS ; TETRABROMOBISPHENOL-A TBBPA ; JUVENILE RAINBOW-TROUT ; GENE-EXPRESSION ; HEPATIC-ENZYMES ; CELL-DEATH ; HBCD ; TRENDS ; MODEL ; FISH
资助信息Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10]
收录类别SCI
语种英语
WOS记录号WOS:000267717800004
公开日期2010-10-13
源URL[http://ir.ihb.ac.cn/handle/152342/7678]  
专题水生生物研究所_中科院水生所知识产出(2009年前)_期刊论文
作者单位1.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China
2.Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China
3.City Univ Hong Kong, Dept Biol & Chem, Hong Kong, Hong Kong, Peoples R China
推荐引用方式
GB/T 7714
Deng, Jun,Yu, Liqin,Liu, Chunsheng,et al. Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos[J]. AQUATIC TOXICOLOGY,2009,93(1):29-36.
APA Deng, Jun.,Yu, Liqin.,Liu, Chunsheng.,Yu, Ke.,Shi, Xiongjie.,...&Zhou, Bingsheng.(2009).Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos.AQUATIC TOXICOLOGY,93(1),29-36.
MLA Deng, Jun,et al."Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos".AQUATIC TOXICOLOGY 93.1(2009):29-36.

入库方式: OAI收割

来源:水生生物研究所

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