File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Hexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos

TitleHexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos
Authors
Issue Date2009
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/aquatox
Citation
Aquatic Toxicology, 2009, v. 93 n. 1, p. 29-36 How to Cite?
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. © 2009 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179136
ISSN
2015 Impact Factor: 3.557
2015 SCImago Journal Rankings: 1.671
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDeng, Jen_US
dc.contributor.authorYu, Len_US
dc.contributor.authorLiu, Cen_US
dc.contributor.authorYu, Ken_US
dc.contributor.authorShi, Xen_US
dc.contributor.authorYeung, LWYen_US
dc.contributor.authorLam, PKSen_US
dc.contributor.authorWu, RSSen_US
dc.contributor.authorZhou, Ben_US
dc.date.accessioned2012-12-19T09:52:16Z-
dc.date.available2012-12-19T09:52:16Z-
dc.date.issued2009en_US
dc.identifier.citationAquatic Toxicology, 2009, v. 93 n. 1, p. 29-36en_US
dc.identifier.issn0166-445Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/179136-
dc.description.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. © 2009 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/aquatoxen_US
dc.relation.ispartofAquatic Toxicologyen_US
dc.subject.meshAbnormalities, Drug-Induced - Etiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effects - Geneticsen_US
dc.subject.meshApoptosis Regulatory Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshEmbryo, Nonmammalian - Drug Effectsen_US
dc.subject.meshFemaleen_US
dc.subject.meshFlame Retardants - Toxicityen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshGene Expression Regulation, Developmental - Drug Effectsen_US
dc.subject.meshHydrocarbons, Brominated - Toxicityen_US
dc.subject.meshMaleen_US
dc.subject.meshRna, Messenger - Biosynthesis - Geneticsen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshZebrafish - Embryology - Geneticsen_US
dc.titleHexabromocyclododecane-induced developmental toxicity and apoptosis in zebrafish embryosen_US
dc.typeArticleen_US
dc.identifier.emailWu, RSS: rudolfwu@hku.hken_US
dc.identifier.authorityWu, RSS=rp01398en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.aquatox.2009.03.001en_US
dc.identifier.pmid19356805-
dc.identifier.scopuseid_2-s2.0-67349142541en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67349142541&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume93en_US
dc.identifier.issue1en_US
dc.identifier.spage29en_US
dc.identifier.epage36en_US
dc.identifier.isiWOS:000267717800004-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridDeng, J=35304700000en_US
dc.identifier.scopusauthoridYu, L=37022805800en_US
dc.identifier.scopusauthoridLiu, C=8318316300en_US
dc.identifier.scopusauthoridYu, K=35757266000en_US
dc.identifier.scopusauthoridShi, X=16067334700en_US
dc.identifier.scopusauthoridYeung, LWY=9735175200en_US
dc.identifier.scopusauthoridLam, PKS=7202365776en_US
dc.identifier.scopusauthoridWu, RSS=7402945079en_US
dc.identifier.scopusauthoridZhou, B=7401906781en_US
dc.identifier.citeulike4814318-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats