MITOCHONDRIAL GENOME DAMAGE ASSOCIATED WITH CIGARETTE-SMOKING

We have investigated the level of mitochondrial DNA (mtDNA) damage and deletions in bronchoalveolar lavage tissues from smokers and nonsmoke rs using quantitative, extra-long PCR and a ''common'' mtDNA deletion assay. Smokers had 5.6 times the level of mtDNA damage, 2.6 times the damage at a nuclear locus (beta-globin gene cluster), and almost 7 tim es the level of a 4.9-kb mtDNA deletion compared to nonsmokers, althou gh the latter increase was not significant. Although both genomes (mit ochondrial and nuclear) showed significantly increased levels of DNA, damage in smokers (mtDNA P = 0.00072; beta-globin P = 0.0056), the rel ative differences were greatest in the mtDNA. Damage to the mtDNA may inhibit oxidative phosphorylation and, therefore, potentially cause or contribute to chronic Lung disease and cancer. Consequently, the mtDN A may be a sensitive biomarker for environmentally induced genetic dam age and mutation.