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Article: Catalase and Peroxiredoxin 5 Protect Xenopus Embryos against Alcohol-Induced Ocular Anomalies

TitleCatalase and Peroxiredoxin 5 Protect Xenopus Embryos against Alcohol-Induced Ocular Anomalies
Authors
Issue Date2004
PublisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org
Citation
Investigative Ophthalmology And Visual Science, 2004, v. 45 n. 1, p. 23-29 How to Cite?
AbstractPURPOSE. To study the molecular mechanisms underlying alcohol-induced ocular anomalies in Xenopus embryos. METHODS. Xenopus embryos were exposed to various concentrations (0.1%-0.5%) of alcohol, and the subsequent effects in eye development and in eye marker gene expression were determined. To investigate the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in fetal alcohol syndrome (FAS)-associated ocular injury, two antioxidant enzymes, catalase and peroxiredoxin 5, were overexpressed in the two blastomeres of the two-cell stage Xenopus embryos. RESULTS. Exposure of Xenopus embryos to alcohol during eye development produced marked gross ocular anomalies, including microphthalmia, incomplete closure of the choroid fissure, and malformation of the retina in 40% of the eyes examined. In parallel, alcohol (0.1%-0.5%) dose dependently and significantly reduced the expression of several eye marker genes, of which TBX5, VAX2, and Pax6 were the most vulnerable. Overexpression of catalase and of cytosolic and mitochondrial peroxiredoxin 5 restored the expression of these alcohol-sensitive eye markers and significantly decreased the frequency of ocular malformation from 39% to 21%, 19%, and 13% respectively. All these enzymes reduced alcohol-induced ROS production, but only peroxiredoxin 5 inhibited RNS formation in the alcohol-treated embryos. CONCLUSIONS. The results suggest that oxidative and nitrosative stresses both contribute to alcohol-induced fetal ocular injury.
Persistent Identifierhttp://hdl.handle.net/10722/149791
ISSN
2015 Impact Factor: 3.427
2015 SCImago Journal Rankings: 2.008
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorYang, PHen_HK
dc.contributor.authorGuo, Yen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorTay, Den_HK
dc.contributor.authorGe, Jen_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCen_HK
dc.date.accessioned2012-06-26T05:58:45Z-
dc.date.available2012-06-26T05:58:45Z-
dc.date.issued2004en_HK
dc.identifier.citationInvestigative Ophthalmology And Visual Science, 2004, v. 45 n. 1, p. 23-29en_HK
dc.identifier.issn0146-0404en_HK
dc.identifier.urihttp://hdl.handle.net/10722/149791-
dc.description.abstractPURPOSE. To study the molecular mechanisms underlying alcohol-induced ocular anomalies in Xenopus embryos. METHODS. Xenopus embryos were exposed to various concentrations (0.1%-0.5%) of alcohol, and the subsequent effects in eye development and in eye marker gene expression were determined. To investigate the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in fetal alcohol syndrome (FAS)-associated ocular injury, two antioxidant enzymes, catalase and peroxiredoxin 5, were overexpressed in the two blastomeres of the two-cell stage Xenopus embryos. RESULTS. Exposure of Xenopus embryos to alcohol during eye development produced marked gross ocular anomalies, including microphthalmia, incomplete closure of the choroid fissure, and malformation of the retina in 40% of the eyes examined. In parallel, alcohol (0.1%-0.5%) dose dependently and significantly reduced the expression of several eye marker genes, of which TBX5, VAX2, and Pax6 were the most vulnerable. Overexpression of catalase and of cytosolic and mitochondrial peroxiredoxin 5 restored the expression of these alcohol-sensitive eye markers and significantly decreased the frequency of ocular malformation from 39% to 21%, 19%, and 13% respectively. All these enzymes reduced alcohol-induced ROS production, but only peroxiredoxin 5 inhibited RNS formation in the alcohol-treated embryos. CONCLUSIONS. The results suggest that oxidative and nitrosative stresses both contribute to alcohol-induced fetal ocular injury.en_HK
dc.languageengen_US
dc.publisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.orgen_HK
dc.relation.ispartofInvestigative Ophthalmology and Visual Scienceen_HK
dc.subject.meshAbnormalities, Drug-Induced - Etiology - Metabolism - Prevention & Controlen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Markers - Analysisen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCatalase - Physiologyen_US
dc.subject.meshChoroid - Abnormalitiesen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEmbryo, Nonmammalian - Drug Effectsen_US
dc.subject.meshEthanol - Toxicityen_US
dc.subject.meshEye Abnormalities - Chemically Induced - Metabolism - Prevention & Controlen_US
dc.subject.meshEye Proteinsen_US
dc.subject.meshHomeodomain Proteins - Genetics - Metabolismen_US
dc.subject.meshMicrophthalmos - Chemically Induced - Metabolism - Prevention & Controlen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshPaired Box Transcription Factorsen_US
dc.subject.meshPeroxidases - Physiologyen_US
dc.subject.meshPeroxiredoxinsen_US
dc.subject.meshReactive Nitrogen Species - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshReactive Oxygen Species - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshRetina - Abnormalitiesen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshT-Box Domain Proteins - Genetics - Metabolismen_US
dc.subject.meshXenopus Proteinsen_US
dc.subject.meshXenopus Laevis - Embryologyen_US
dc.titleCatalase and Peroxiredoxin 5 Protect Xenopus Embryos against Alcohol-Induced Ocular Anomaliesen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailTay, D: dkctay@hkucc.hku.hken_HK
dc.identifier.emailLin, MC: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityTay, D=rp00336en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1167/iovs.03-0550en_HK
dc.identifier.pmid14691149-
dc.identifier.scopuseid_2-s2.0-9144258564en_HK
dc.identifier.hkuros86194-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9144258564&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume45en_HK
dc.identifier.issue1en_HK
dc.identifier.spage23en_HK
dc.identifier.epage29en_HK
dc.identifier.isiWOS:000187875600004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridYang, PH=24340289000en_HK
dc.identifier.scopusauthoridGuo, Y=8555122500en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridLiu, J=36014680100en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridTay, D=55392935900en_HK
dc.identifier.scopusauthoridGe, J=25421653600en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK

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