pubmed-article:16094661 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0544886 | lld:lifeskim |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0205332 | lld:lifeskim |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0870883 | lld:lifeskim |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0043902 | lld:lifeskim |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:16094661 | lifeskim:mentions | umls-concept:C0047001 | lld:lifeskim |
pubmed-article:16094661 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:16094661 | pubmed:dateCreated | 2006-1-12 | lld:pubmed |
pubmed-article:16094661 | pubmed:abstractText | Xpc-null (Xpc-/-) mice, deficient in the global genome repair subpathway of nucleotide excision repair (NER-GGR), were exposed by intraperitoneal (i.p.) injection to a 300 mg/kg mutagenic dose of 3,4-epoxy-1-butene (EB), to investigate NER's potential role in repairing butadiene (BD) epoxide DNA lesions. Mutagenic sensitivity was assessed using the Hprt assay. Xpc-/- mice were significantly more sensitive to EB exposure, exhibiting an average 2.8-fold increase in Hprt mutant frequency (MF) relative to those of exposed Xpc+/+ (wild-type) mice. As a positive control for NER-GGR, additional mice were exposed by i.p. injection to a 150 mg/kg mutagenic dose of benzo[a]pyrene (B[a]P). The Xpc-/- mice had MFs 2.9-fold higher than those of exposed Xpc+/+ mice. These results suggest that NER-GGR plays a role in recognizing and repairing some of the DNA adducts formed following in vivo exposure to EB. Additional research is needed to examine the response of Xpc-/- mice, as well as other NER-deficient strains, to inhaled BD. Furthermore, it is likely that alternative DNA repair pathways also are involved in restoring genomic integrity compromised by BD-epoxide DNA damage. Collaborative studies are currently underway to address these critical issues. | lld:pubmed |
pubmed-article:16094661 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:language | eng | lld:pubmed |
pubmed-article:16094661 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16094661 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16094661 | pubmed:month | Jan | lld:pubmed |
pubmed-article:16094661 | pubmed:issn | 0893-6692 | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:LloydR SRS | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:FriedbergE... | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:WardJ BJBJr | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:AmmenheuserM... | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:XieJJ | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:HerringS MSM | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:WickliffeJ... | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:GalbertL ALA | lld:pubmed |
pubmed-article:16094661 | pubmed:author | pubmed-author:MastersO... | lld:pubmed |
pubmed-article:16094661 | pubmed:copyrightInfo | 2005 Wiley-Liss, Inc. | lld:pubmed |
pubmed-article:16094661 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16094661 | pubmed:volume | 47 | lld:pubmed |
pubmed-article:16094661 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16094661 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16094661 | pubmed:pagination | 67-70 | lld:pubmed |
pubmed-article:16094661 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:16094661 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16094661 | pubmed:articleTitle | 3,4-Epoxy-1-butene, a reactive metabolite of 1,3-butadiene, induces somatic mutations in Xpc-null mice. | lld:pubmed |
pubmed-article:16094661 | pubmed:affiliation | Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, Texas, USA. jkwickli@utmb.edu | lld:pubmed |
pubmed-article:16094661 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16094661 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:16094661 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |