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dc.contributor.authorRisom, Lotte
dc.contributor.authorLundby, Carsten
dc.contributor.authorThomsen, Jonas Juhl
dc.contributor.authorMikkelsen, Lone
dc.contributor.authorLoft, Steffen
dc.contributor.authorFriis, Gitte
dc.contributor.authorMoller, Peter
dc.date.accessioned2008-09-04T09:01:02Z
dc.date.available2008-09-04T09:01:02Z
dc.date.issued2007-12-01
dc.identifier.citationMutat. Res. 2007, 625 (1-2):125-133en
dc.identifier.issn0027-5107
dc.identifier.pmid17644143
dc.identifier.doi10.1016/j.mrfmmm.2007.06.001
dc.identifier.urihttp://hdl.handle.net/10146/37173
dc.description.abstractResearch indicates that exposure to hypoxia is associated with oxidative stress. In this investigation, healthy subjects were exposed to hypoxia by inhalation of 10% oxygen for 2h (corresponding to 5500m above sea level). The levels of strand breaks and oxidatively damaged purine bases, measured by the comet assay, and the expression of genes involved in DNA repair of oxidatively damaged DNA were investigated in mononuclear blood cells (MNBC) at baseline, after 2h of hypoxia, 2h of reoxygenation, and 1 day and 8 days after the exposure. The level of strand breaks and oxidized purine bases in MNBC increased following both the 2h of hypoxia and the 2h reoxygenation period, whereas this effect was not observed in unexposed subjects. The expressions of oxoguanine DNA glycosylase 1 (OGG1), nucleoside diphosphate linked moiety X-type motif 1 (NUDT1), nei endonuclease VIII-like 1 (NEIL1), and mutY homolog (MUTYH) were unaltered throughout the experiment in both groups of subjects, indicating that DNA repair genes are not up-regulated by the hypoxia and reoxygenation treatment. Taken together, this report shows that inhalation of 10% oxygen for 2h is associated with increased number of oxidized DNA lesions in MNBC, but acute hypoxia may not inflict upon the regulation of genes involved in repair of oxidized DNA.
dc.description.sponsorshipThis study was supported by the Danish Research Agency. The authors (L.R., L.M., S.L., G.F., and P.M.) of this paper are partners of ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5: “Food Quality and Safety” (Contract No. 513943).en
dc.language.isoenen
dc.relation.urlhttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2C-4NYSXWR-1&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=1843694&md5=bac0fdcafb9dbd3f60202229312e6a33en
dc.subjectComet assayen
dc.subjectDNA repairen
dc.subjectGene expressionen
dc.subjectOxidative DNA damageen
dc.subject.meshAdult
dc.subject.meshAnoxia
dc.subject.meshBase Sequence
dc.subject.meshComet Assay
dc.subject.meshDNA Damage
dc.subject.meshDNA Glycosylases
dc.subject.meshDNA Primers
dc.subject.meshDNA Repair
dc.subject.meshDNA Repair Enzymes
dc.subject.meshFemale
dc.subject.meshGene Expression
dc.subject.meshHumans
dc.subject.meshLeukocytes, Mononuclear
dc.subject.meshMale
dc.subject.meshOxidative Stress
dc.subject.meshPhosphoric Monoester Hydrolases
dc.subject.meshRNA, Messenger
dc.titleAcute hypoxia and reoxygenation-induced DNA oxidation in human mononuclear blood cells.en
dc.typeArticleen
dc.identifier.journalMutation Researchen
html.description.abstractResearch indicates that exposure to hypoxia is associated with oxidative stress. In this investigation, healthy subjects were exposed to hypoxia by inhalation of 10% oxygen for 2h (corresponding to 5500m above sea level). The levels of strand breaks and oxidatively damaged purine bases, measured by the comet assay, and the expression of genes involved in DNA repair of oxidatively damaged DNA were investigated in mononuclear blood cells (MNBC) at baseline, after 2h of hypoxia, 2h of reoxygenation, and 1 day and 8 days after the exposure. The level of strand breaks and oxidized purine bases in MNBC increased following both the 2h of hypoxia and the 2h reoxygenation period, whereas this effect was not observed in unexposed subjects. The expressions of oxoguanine DNA glycosylase 1 (OGG1), nucleoside diphosphate linked moiety X-type motif 1 (NUDT1), nei endonuclease VIII-like 1 (NEIL1), and mutY homolog (MUTYH) were unaltered throughout the experiment in both groups of subjects, indicating that DNA repair genes are not up-regulated by the hypoxia and reoxygenation treatment. Taken together, this report shows that inhalation of 10% oxygen for 2h is associated with increased number of oxidized DNA lesions in MNBC, but acute hypoxia may not inflict upon the regulation of genes involved in repair of oxidized DNA.


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