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Article: Ascorbic acid inhibits ROS production, NF-κB activation and prevents ethanol-induced growth retardation and microencephaly

TitleAscorbic acid inhibits ROS production, NF-κB activation and prevents ethanol-induced growth retardation and microencephaly
Authors
KeywordsAscorbic acid
Ethanol
Fetal development
Xenopus laevis
Issue Date2005
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm
Citation
Neuropharmacology, 2005, v. 48 n. 3, p. 426-434 How to Cite?
AbstractIn this study, we established an embryo model to study the effects of ethanol on fetal development. When embryos of Xenopus laevis (the African clawed frog) were exposed to ethanol, the resultant tadpoles had significantly reduced brain sizes (microencephaly) and retarded growth rates. These effects, similar to those observed in human fetal alcohol syndrome (FAS), were dose- and time-dependent. We further showed that the antioxidant ascorbic acid (vitamin C) could inhibit the ethanol-induced reactive oxygen species (ROS) production and NF-κB activation and protect the ethanol-treated embryos against microencephaly and growth retardation. These results suggest the involvement of NF-κB and oxidative stress in ethanol-mediated developmental defects, and the potential use of ascorbic acid as a new and effective protective agent for FAS. © 2004 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/167893
ISSN
2015 Impact Factor: 4.936
2015 SCImago Journal Rankings: 2.506
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorKwok, KHHen_HK
dc.contributor.authorYang, PHen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorWong, OGen_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCMen_HK
dc.date.accessioned2012-10-08T03:12:37Z-
dc.date.available2012-10-08T03:12:37Z-
dc.date.issued2005en_HK
dc.identifier.citationNeuropharmacology, 2005, v. 48 n. 3, p. 426-434en_HK
dc.identifier.issn0028-3908en_HK
dc.identifier.urihttp://hdl.handle.net/10722/167893-
dc.description.abstractIn this study, we established an embryo model to study the effects of ethanol on fetal development. When embryos of Xenopus laevis (the African clawed frog) were exposed to ethanol, the resultant tadpoles had significantly reduced brain sizes (microencephaly) and retarded growth rates. These effects, similar to those observed in human fetal alcohol syndrome (FAS), were dose- and time-dependent. We further showed that the antioxidant ascorbic acid (vitamin C) could inhibit the ethanol-induced reactive oxygen species (ROS) production and NF-κB activation and protect the ethanol-treated embryos against microencephaly and growth retardation. These results suggest the involvement of NF-κB and oxidative stress in ethanol-mediated developmental defects, and the potential use of ascorbic acid as a new and effective protective agent for FAS. © 2004 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharmen_HK
dc.relation.ispartofNeuropharmacologyen_HK
dc.subjectAscorbic aciden_HK
dc.subjectEthanolen_HK
dc.subjectFetal developmenten_HK
dc.subjectXenopus laevisen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshAscorbic Acid - Pharmacology - Therapeutic Useen_US
dc.subject.meshEthanol - Antagonists & Inhibitors - Toxicityen_US
dc.subject.meshFetal Growth Retardation - Chemically Induced - Prevention & Controlen_US
dc.subject.meshMicrocephaly - Chemically Induced - Prevention & Controlen_US
dc.subject.meshNf-Kappa B - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshReactive Oxygen Species - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshXenopus Laevisen_US
dc.titleAscorbic acid inhibits ROS production, NF-κB activation and prevents ethanol-induced growth retardation and microencephalyen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neuropharm.2004.10.018en_HK
dc.identifier.pmid15721175-
dc.identifier.scopuseid_2-s2.0-13844275277en_HK
dc.identifier.hkuros105168-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-13844275277&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume48en_HK
dc.identifier.issue3en_HK
dc.identifier.spage426en_HK
dc.identifier.epage434en_HK
dc.identifier.isiWOS:000227622600012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridKwok, KHH=7102194193en_HK
dc.identifier.scopusauthoridYang, PH=24340289000en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridLiu, J=36014680100en_HK
dc.identifier.scopusauthoridWong, OG=7004813981en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK

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