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Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos
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; Zhou, BS, Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Donghu S Rd 7, Wuhan 430072, Peoples R China
2009-06-04
Source PublicationAQUATIC TOXICOLOGY
ISSN0166-445X
Volume93Issue:1Pages:29-36
AbstractHexabromocyclododecane (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.; 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.
SubtypeArticle
KeywordHbcd Developmental Toxicity Apoptosis Zebrafish Embryo Gene Expression
Department[Deng, Jun; Yu, Liqin; Liu, Chunsheng; Yu, Ke; Shi, Xiongjie; Zhou, Bingsheng] Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China; [Deng, Jun; Yu, Liqin] Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China; [Yeung, Leo W. Y.; Lam, Paul K. S.; Wu, Rudolf S. S.] City Univ Hong Kong, Dept Biol & Chem, Hong Kong, Hong Kong, Peoples R China
Subject AreaMarine & Freshwater Biology ; Toxicology
DOI10.1016/j.aquatox.2009.03.001
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Funding OrganizationMinistry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] ; Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] ; Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] ; Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10]
Indexed BySCI
Language英语
WOS Research AreaMarine & Freshwater Biology ; Toxicology
WOS SubjectMarine & Freshwater Biology ; Toxicology
WOS IDWOS:000267717800004
WOS KeywordBROMINATED FLAME RETARDANTS ; TETRABROMOBISPHENOL-A TBBPA ; JUVENILE RAINBOW-TROUT ; GENE-EXPRESSION ; HEPATIC-ENZYMES ; CELL-DEATH ; HBCD ; TRENDS ; MODEL ; FISH
Funding OrganizationMinistry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] ; Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] ; Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10] ; Ministry of Science and Technology of China [2006AA06Z420]; National Nature Science Foundation of China [20890113]; State Key Laboratory of Freshwater Ecology and Biotechnology [2008FBZ10]
Citation statistics
Cited Times:136[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/152342/7678
Collection期刊论文
Corresponding AuthorZhou, BS, Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Donghu S Rd 7, Wuhan 430072, Peoples R China
Affiliation1.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
Recommended Citation
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, BS, Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Donghu S Rd 7, Wuhan 430072, Peoples R China.(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.
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