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Article: An embryoprotective role for glucose-6-phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis

TitleAn embryoprotective role for glucose-6-phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis
Authors
KeywordsBirth defects
Development
Human risk
Phenytoin
Reactive oxygen species
Issue Date2000
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 2000, v. 14 n. 1, p. 111-127 How to Cite?
AbstractThe primary recognized health risk from common deficiencies in glucose- 6-phosphate dehydrogenase (G6PD), a cytoprotective enzyme for oxidative stress, is red blood cell hemolysis. Here we show that litters from untreated pregnant mutant mice with a hereditary G6PD deficiency had increased prenatal (fetal resorptions) and postnatal death. When treated with the anticonvulsant drug phenytoin, a human teratogen that is commonly used in pregnant women and causes embryonic oxidative stress, G6PD-deficient dams had higher embryonic DNA oxidation and more fetal death and birth defects. The reported G6PD gene mutation was confirmed and used to genotype fetal resorptions, which were primarily G6PD deficient. This is the first evidence that G6PD is a developmentally critical cytoprotective enzyme for both endogenous and xenobiotic-initiated embryopathic oxidative stress and DNA damage. G6PD deficiencies accordingly may have a broader biological relevance as important determinants of infertility, in utero and postnatal death, and teratogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/44357
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775
Other Identifiers
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNicol, CJen_HK
dc.contributor.authorZielenski, Jen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorWells, PGen_HK
dc.date.accessioned2007-09-12T03:52:02Z-
dc.date.available2007-09-12T03:52:02Z-
dc.date.issued2000en_HK
dc.identifierhttp://www.fasebj.org/cgi/reprint/14/1/111en_HK
dc.identifier.citationFaseb Journal, 2000, v. 14 n. 1, p. 111-127en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/44357-
dc.description.abstractThe primary recognized health risk from common deficiencies in glucose- 6-phosphate dehydrogenase (G6PD), a cytoprotective enzyme for oxidative stress, is red blood cell hemolysis. Here we show that litters from untreated pregnant mutant mice with a hereditary G6PD deficiency had increased prenatal (fetal resorptions) and postnatal death. When treated with the anticonvulsant drug phenytoin, a human teratogen that is commonly used in pregnant women and causes embryonic oxidative stress, G6PD-deficient dams had higher embryonic DNA oxidation and more fetal death and birth defects. The reported G6PD gene mutation was confirmed and used to genotype fetal resorptions, which were primarily G6PD deficient. This is the first evidence that G6PD is a developmentally critical cytoprotective enzyme for both endogenous and xenobiotic-initiated embryopathic oxidative stress and DNA damage. G6PD deficiencies accordingly may have a broader biological relevance as important determinants of infertility, in utero and postnatal death, and teratogenesis.en_HK
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_HK
dc.relation.ispartofFASEB Journalen_HK
dc.subjectBirth defectsen_HK
dc.subjectDevelopmenten_HK
dc.subjectHuman risken_HK
dc.subjectPhenytoinen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subject.meshEmbryo - drug effectsen_HK
dc.subject.meshEmbryonic and Fetal Development - physiologyen_HK
dc.subject.meshGlucosephosphate Dehydrogenase - physiologyen_HK
dc.subject.meshOxidative Stressen_HK
dc.subject.meshTeratogens - pharmacologyen_HK
dc.titleAn embryoprotective role for glucose-6-phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesisen_HK
dc.typeArticleen_HK
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.pmid10627286-
dc.identifier.scopuseid_2-s2.0-0033977661en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033977661&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue1en_HK
dc.identifier.spage111en_HK
dc.identifier.epage127en_HK
dc.identifier.isiWOS:000084784700014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNicol, CJ=35445014900en_HK
dc.identifier.scopusauthoridZielenski, J=7003732699en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridWells, PG=7201752649en_HK

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