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Oxidatively damaged DNA and its repair after experimental exposure to wood smoke in healthy humans.

Journal article
Authors Pernille Hogh Danielsen
Elvira Vaclavik Bräuner
Lars Barregård
Gerd Sällsten
Maria Wallin
Ryszard Olinski
Rafal Rozalski
Peter Moller
Steffen Loft
Published in Mutation research
Volume 642
Issue 1-2
Pages 37-42
ISSN 0027-5107
Publication year 2008
Published at Institute of Medicine, School of Public Health and Community Medicine
Pages 37-42
Language en
Keywords Air Pollutants, adverse effects, DNA Damage, DNA Glycosylases, blood, DNA Repair, Humans, Leukocytes, Mononuclear, chemistry, Oxidative Stress, Smoke, adverse effects, Wood
Subject categories Public health medicine research areas


Particulate matter from wood smoke may cause health effects through generation of oxidative stress with resulting damage to DNA. We investigated oxidatively damaged DNA and related repair capacity in peripheral blood mononuclear cells (PBMC) and measured the urinary excretion of repair products after controlled short-term exposure of human volunteers to wood smoke. Thirteen healthy adults were exposed first to clean air and then to wood smoke in a chamber during 4h sessions, 1 week apart. Blood samples were taken 3h after exposure and on the following morning, and urine was collected after exposure, from bedtime until the next morning. We measured the levels of DNA strand breaks (SB), oxidized purines as formamidopyrimidine-DNA-glycosylase (FPG) sites and activity of oxoguanine glycosylase 1 (hOGG1) in PBMC by the comet assay, whereas mRNA levels of hOGG1, nucleoside diphosphate linked moiety X-type motif 1 (hNUDT1) and heme oxygenase 1 (hHO1) were determined by real-time RT-PCR. The excretion of 8-oxo-7,8-dihydro-oxoguanine (8-oxoGua) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine was measured by high performance liquid chromatography purification followed by gas chromatography with mass spectrometry. The morning following exposure to wood smoke the PBMC levels of SB were significantly decreased and the mRNA levels of hOGG1 significantly increased. FPG sites, hOGG1 activity, expression of hNUDT1 and hHO1, urinary excretion of 8-oxodG and 8-oxoGua did not change significantly. Our findings support that exposure to wood smoke causes systemic effects, although we could not demonstrate genotoxic effects, possibly explained by enhanced repair and timing of sampling.

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