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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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