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dc.contributor.authorDanielsen, Pernille Hogh
dc.contributor.authorRisom, Lotte
dc.contributor.authorWallin, Hakan
dc.contributor.authorAutrup, Herman
dc.contributor.authorVogel, Ulla
dc.contributor.authorLoft, Steffen
dc.contributor.authorMoller, Peter
dc.date.accessioned2008-07-14T11:30:26Z
dc.date.available2008-07-14T11:30:26Z
dc.date.issued2008-01-01
dc.identifier.citationMutat. Res. 2008, 637 (1-2):49-55en
dc.identifier.issn0027-5107
dc.identifier.pmid17764705
dc.identifier.doi10.1016/j.mrfmmm.2007.06.011
dc.identifier.urihttp://hdl.handle.net/10146/31862
dc.description.abstractThe gastrointestinal route of exposure to particulate matter is important because particles are ingested via contaminated foods and inhaled particles are swallowed when removed from the airways by the mucociliary clearance system. We investigated the effect of an intragastric administration by oral gavage of diesel exhaust particles (DEP) in terms of DNA damage, oxidative stress and DNA repair in colon epithelial cells, liver, and lung of rats. Eight rats per group were exposed to Standard Reference Material 2975 at 0.064 or 0.64 mg/kg bodyweight for 6 and 24 h. Increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine lesions were observed at the highest dose after 6 and 24 h in all three organs. 8-Oxo-7,8-dihydro-2'-deoxyguanosine is repaired by oxoguanine DNA glycosylase 1 (OGG1); upregulation of this repair system was observed as elevated pulmonary OGG1 mRNA levels after 24 h at both doses of DEP, but not in the colon and liver. A general response of the antioxidant defence system is further indicated by elevated levels of heme oxygenase 1 mRNA in the liver and lung 24 h after administration. The level of bulky DNA adducts was increased in liver and lung at both doses after 6 and 24h (DNA adducts in colon epithelium were not investigated). In summary, DEP administered via the gastrointestinal tract at low doses relative to ambient exposure generates DNA damage and increase the expression of defence mechanisms in organs such as the lung and liver. The oral exposure route should be taken into account in risk assessment of particulate matter.
dc.description.sponsorshipThe work was partly supported by 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) and the Danish Research Councils.en
dc.language.isoenen
dc.relation.urlhttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2C-4P59XK0-2&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=368dc2dc7b34a0dca961dce467421ddden
dc.subjectair pollutionen
dc.subjectDiesel exhaust particlesen
dc.subjectOGG1en
dc.subjectGene expressionen
dc.subject8-oxodGen
dc.subjectHO-1en
dc.subjectPolycyclic aromatic hydrocarbonsen
dc.subjectOxidative stressen
dc.subjectOral exposureen
dc.subjectoxoguanine DNA glycosylase 1en
dc.subjectheme oxygenase 1en
dc.subjectDEPen
dc.subject8-oxo-7,8-dihydro-2′-deoxyguanosineen
dc.subject.meshAdministration, Oral
dc.subject.meshAnimals
dc.subject.meshColon
dc.subject.meshDNA Adducts
dc.subject.meshDNA Damage
dc.subject.meshDNA Glycosylases
dc.subject.meshDNA Repair
dc.subject.meshHeme Oxygenase (Decyclizing)
dc.subject.meshLiver
dc.subject.meshLung
dc.subject.meshMale
dc.subject.meshMutagens
dc.subject.meshOxidative Stress
dc.subject.meshParticulate Matter
dc.subject.meshRats
dc.subject.meshRats, Inbred F344
dc.subject.meshReactive Oxygen Species
dc.subject.meshVehicle Emissions
dc.titleDNA damage in rats after a single oral exposure to diesel exhaust particles.en
dc.typeArticleen
dc.identifier.journalMutation Research. Fundamental and Molecular Mechanisms of Mutagenesisen
html.description.abstractThe gastrointestinal route of exposure to particulate matter is important because particles are ingested via contaminated foods and inhaled particles are swallowed when removed from the airways by the mucociliary clearance system. We investigated the effect of an intragastric administration by oral gavage of diesel exhaust particles (DEP) in terms of DNA damage, oxidative stress and DNA repair in colon epithelial cells, liver, and lung of rats. Eight rats per group were exposed to Standard Reference Material 2975 at 0.064 or 0.64 mg/kg bodyweight for 6 and 24 h. Increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine lesions were observed at the highest dose after 6 and 24 h in all three organs. 8-Oxo-7,8-dihydro-2'-deoxyguanosine is repaired by oxoguanine DNA glycosylase 1 (OGG1); upregulation of this repair system was observed as elevated pulmonary OGG1 mRNA levels after 24 h at both doses of DEP, but not in the colon and liver. A general response of the antioxidant defence system is further indicated by elevated levels of heme oxygenase 1 mRNA in the liver and lung 24 h after administration. The level of bulky DNA adducts was increased in liver and lung at both doses after 6 and 24h (DNA adducts in colon epithelium were not investigated). In summary, DEP administered via the gastrointestinal tract at low doses relative to ambient exposure generates DNA damage and increase the expression of defence mechanisms in organs such as the lung and liver. The oral exposure route should be taken into account in risk assessment of particulate matter.


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