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Article: Protection of Xenopus laevis embryos against alcohol-induced delayed gut maturation and growth retardation by peroxiredoxin 5 and catalase

TitleProtection of Xenopus laevis embryos against alcohol-induced delayed gut maturation and growth retardation by peroxiredoxin 5 and catalase
Authors
Keywordsalcohol
catalase
FAS, fetal alcohol syndrome
gut
NF, Nieuwkoop & Faber
peroxiredoxin 5
PRDX5, peroxiredoxin 5
RNS, reactive nitrogen species
ROS, reactive oxygen species
Xenopus embryos
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/jmb
Citation
Journal Of Molecular Biology, 2004, v. 340 n. 4, p. 819-827 How to Cite?
AbstractAccumulated evidence indicates that maternal alcohol consumption causes fetal enteric damage and growth retardation. In this study, we investigated the underlying molecular mechanisms in a Xenopus model of fetal alcohol exposure. We established a condition of transient alcohol exposure that produces tadpoles with delayed gut maturation and decreased body length. We then investigated the roles of reactive oxygen species (ROS) and reactive nitrogen species (RNS) by microinjecting plasmids expressing catalase and peroxiredoxin 5 (PRDX5) into two-cell stage embryos. Finally, the effects of these enzymes on the expression of key gut developmental genes were determined by animal cap explant assay. We showed that exposure of Xenopus embryos to 0.5% alcohol from stage 13 to stage 22 produced tadpoles with delayed gut maturation, reduced growth, and down-regulation in several gut developmental genes, with VegT, Pax6 and Sox17 most vulnerable. We further demonstrated that microinjection of catalase attenuated alcohol-induced ROS production and restored the expression of VegT and Pax6, but protected the embryos from delayed gut development and retarded growth only partially. By contrast, microinjection of PRDX5 reduced both ROS and RNS production, and prevented the gut and growth defects, and restored VegT, Pax6 and Sox17 gene expression. A positive correlation was found between delayed gut maturation and reduced body length. These results indicate the crucial roles of both the ROS-Pax6 and RNS-Sox17 signaling axes in alcohol-induced fetal gut defects and growth retardation. In addition, they suggest strongly a cause-and-effect relationship between alcohol-induced delayed gut maturation and growth retardation. © 2004 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/88034
ISSN
2015 Impact Factor: 4.517
2015 SCImago Journal Rankings: 3.002
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorYang, PHen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorLum, CTen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCen_HK
dc.date.accessioned2010-09-06T09:37:47Z-
dc.date.available2010-09-06T09:37:47Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Molecular Biology, 2004, v. 340 n. 4, p. 819-827en_HK
dc.identifier.issn0022-2836en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88034-
dc.description.abstractAccumulated evidence indicates that maternal alcohol consumption causes fetal enteric damage and growth retardation. In this study, we investigated the underlying molecular mechanisms in a Xenopus model of fetal alcohol exposure. We established a condition of transient alcohol exposure that produces tadpoles with delayed gut maturation and decreased body length. We then investigated the roles of reactive oxygen species (ROS) and reactive nitrogen species (RNS) by microinjecting plasmids expressing catalase and peroxiredoxin 5 (PRDX5) into two-cell stage embryos. Finally, the effects of these enzymes on the expression of key gut developmental genes were determined by animal cap explant assay. We showed that exposure of Xenopus embryos to 0.5% alcohol from stage 13 to stage 22 produced tadpoles with delayed gut maturation, reduced growth, and down-regulation in several gut developmental genes, with VegT, Pax6 and Sox17 most vulnerable. We further demonstrated that microinjection of catalase attenuated alcohol-induced ROS production and restored the expression of VegT and Pax6, but protected the embryos from delayed gut development and retarded growth only partially. By contrast, microinjection of PRDX5 reduced both ROS and RNS production, and prevented the gut and growth defects, and restored VegT, Pax6 and Sox17 gene expression. A positive correlation was found between delayed gut maturation and reduced body length. These results indicate the crucial roles of both the ROS-Pax6 and RNS-Sox17 signaling axes in alcohol-induced fetal gut defects and growth retardation. In addition, they suggest strongly a cause-and-effect relationship between alcohol-induced delayed gut maturation and growth retardation. © 2004 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/jmben_HK
dc.relation.ispartofJournal of Molecular Biologyen_HK
dc.subjectalcoholen_HK
dc.subjectcatalaseen_HK
dc.subjectFAS, fetal alcohol syndromeen_HK
dc.subjectguten_HK
dc.subjectNF, Nieuwkoop & Faberen_HK
dc.subjectperoxiredoxin 5en_HK
dc.subjectPRDX5, peroxiredoxin 5en_HK
dc.subjectRNS, reactive nitrogen speciesen_HK
dc.subjectROS, reactive oxygen speciesen_HK
dc.subjectXenopus embryosen_HK
dc.titleProtection of Xenopus laevis embryos against alcohol-induced delayed gut maturation and growth retardation by peroxiredoxin 5 and catalaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2836&volume=340&spage=819&epage=827&date=2004&atitle=Protection+of+Xenopus+laevis+embryos+against+alcohol-induced+delayed+gut+maturation+and+growth+retardation+by+peroxiredoxin+5+and+catalaseen_HK
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailLum, CT: lumct@hku.hken_HK
dc.identifier.emailLin, MC: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityLum, CT=rp00757en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jmb.2004.05.047en_HK
dc.identifier.pmid15223323-
dc.identifier.scopuseid_2-s2.0-3042515687en_HK
dc.identifier.hkuros91810en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3042515687&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume340en_HK
dc.identifier.issue4en_HK
dc.identifier.spage819en_HK
dc.identifier.epage827en_HK
dc.identifier.isiWOS:000222734300014-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridYang, PH=24340289000en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridLum, CT=7006889374en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK

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