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dc.contributor.authorNukui, Tomoko
dc.contributor.authorDay, Richard D.
dc.contributor.authorGordish-Dressman, Heather A.
dc.contributor.authorHarger, Gail
dc.contributor.authorBigbee, William L.
dc.contributor.authorNess, Roberta B.
dc.contributor.authorRomkes, Marjorie
dc.date.accessioned2009-03-24T09:47:33Z
dc.date.available2009-03-24T09:47:33Z
dc.date.issued2006-02
dc.identifier.citationPharmacogenet. Genomics 2006, 16 (2):129-138en
dc.identifier.issn1744-6872
dc.identifier.pmid16424825
dc.identifier.urihttp://hdl.handle.net/10146/56957
dc.description. Biomarkers of exposure & early effects: field studiesBiomarker: mutation frequency of glycophorin AExposure/effect represented: cigarette smoke/ DNA damageStudy design: cross-sectionalStudy size: 2405 pregnant womenAnalytical technique: The GPA somatic cell mutation assayTissue/biological material/sample size: peripheral bloodImpact on outcome (including dose-response): active smoker/non-smoker a positive significant overall association of smoking with a newborn Ψ/N Vf was observed by generalized linear model analysis (P=0.023)Quality control: reliability of maternal self-reported cigarette smoking was verified by measuring cotinine levels in maternal blood samples in a separate analysisBiomarkers of individual susceptibility: field studiesBiomarker (including alleles if genetic): CYP1A1*2A, CYP1A1*3, CYP2E1*5B, NAT2*5, *6A, *7A and *14A, GSTM1 and GSTT1Effect studied (phenotype/pathology): DNA damageMethod of analysis: RFLP-PCRImpact on outcome (including dose-response): CYP1A1* 2A or CYP1A1*3, 33.6%; CYP2E1*5B, 6.9%; GSTM1 null, 46.8%; GSTT1 null, 24.1%; and NAT2 slow, 43.1%. KEYWORDS CLASSIFICATION: Adolescent;Adult;Alleles;biomarkers of exposure & effect: field studies;biomarkers of individual susceptibility: field studies;blood;Female;Fetal Blood;genetics;Genotype;Glycophorin;Humans;Infant,Newborn;metabolism;methods;Maternal-Fetal Exchange;Mothers;Mutation;Pharmacogenetics;Polymorphism,Genetic;Pregnancy;Research;Smoking.en
dc.description.abstractPrenatal exposure to carcinogens results in newborn DNA damage which in turn is associated with impaired health conditions in both childhood and adulthood. The present study aimed to evaluate whether phase I and II biotransformation enzyme genetic polymorphisms in combination with environmental exposures during pregnancy result in elevated levels of newborn DNA damage. Maternal peripheral and umbilical cord blood samples from 406 mother/newborn pairs were genotyped for a panel of phase I/II metabolic enzymes (CYP1A1, CYP2E1, GSTM1, GSTT1 and NAT2) responsible for the metabolism of tobacco and lifestyle-related mutagens and carcinogens. DNA damage was measured by somatic cell mutation frequency at the glycophorin A (GPA) locus in newborns. No association with elevated somatic cell mutation frequency was observed between the combination of maternal/newborn genotypes and cigarette smoke or lifestyle exposures. The observed variation in newborn GPA frequency might be due to either environmental factors not assessed in this study or inter-individual differences in alternative metabolic or DNA repair pathways.
dc.language.isoenen
dc.relation.urlhttp://www.jpharmacogenetics.com/pt/re/pharmgen/abstract.01213011-200602000-00007.htm;jsessionid=JLrc3YrxLySCtJybR9pMlbQZY7t0MLKR9grQM11fwCPLGwhkBFZr!-269263472!181195628!8091!-1en
dc.subject.meshAdolescent
dc.subject.meshAdult
dc.subject.meshAlleles
dc.subject.meshFemale
dc.subject.meshFetal Blood
dc.subject.meshGenotype
dc.subject.meshGlycophorin
dc.subject.meshHumans
dc.subject.meshInfant, Newborn
dc.subject.meshMaternal-Fetal Exchange
dc.subject.meshMothers
dc.subject.meshMutation
dc.subject.meshPharmacogenetics
dc.subject.meshPolymorphism, Genetic
dc.subject.meshPregnancy
dc.subject.meshSmoking
dc.titleThe absence of interaction between drug metabolizing enzyme genotypes and maternal lifestyle factors on glycophorin A somatic mutation frequency levels in newborns.en
dc.typeArticleen
dc.identifier.journalPharmacogenetics and genomicsen
html.description.abstractPrenatal exposure to carcinogens results in newborn DNA damage which in turn is associated with impaired health conditions in both childhood and adulthood. The present study aimed to evaluate whether phase I and II biotransformation enzyme genetic polymorphisms in combination with environmental exposures during pregnancy result in elevated levels of newborn DNA damage. Maternal peripheral and umbilical cord blood samples from 406 mother/newborn pairs were genotyped for a panel of phase I/II metabolic enzymes (CYP1A1, CYP2E1, GSTM1, GSTT1 and NAT2) responsible for the metabolism of tobacco and lifestyle-related mutagens and carcinogens. DNA damage was measured by somatic cell mutation frequency at the glycophorin A (GPA) locus in newborns. No association with elevated somatic cell mutation frequency was observed between the combination of maternal/newborn genotypes and cigarette smoke or lifestyle exposures. The observed variation in newborn GPA frequency might be due to either environmental factors not assessed in this study or inter-individual differences in alternative metabolic or DNA repair pathways.


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