Linked Life Data

15223323

Source:http://linkedlifedata.com/resource/pubmed/id/15223323

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-6-29
pubmed:abstractText
Accumulated 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-2836
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
340
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
819-27
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15223323-Animals, pubmed-meshheading:15223323-Antioxidants, pubmed-meshheading:15223323-Biological Markers, pubmed-meshheading:15223323-Catalase, pubmed-meshheading:15223323-Culture Techniques, pubmed-meshheading:15223323-Digestive System, pubmed-meshheading:15223323-Embryo, Nonmammalian, pubmed-meshheading:15223323-Ethanol, pubmed-meshheading:15223323-Female, pubmed-meshheading:15223323-Gene Expression Regulation, Developmental, pubmed-meshheading:15223323-Microinjections, pubmed-meshheading:15223323-Peroxidases, pubmed-meshheading:15223323-Peroxiredoxins, pubmed-meshheading:15223323-Reactive Nitrogen Species, pubmed-meshheading:15223323-Reactive Oxygen Species, pubmed-meshheading:15223323-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15223323-Xenopus laevis
pubmed:year
2004
pubmed:articleTitle
Protection of Xenopus laevis embryos against alcohol-induced delayed gut maturation and growth retardation by peroxiredoxin 5 and catalase.
pubmed:affiliation
Institute of Molecular Biology and Open Lab of Chemical Biology, Institute of Molecular Technology for Drug Discovery and Synthesis, University of Hong Kong, Hong Kong, China.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't