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Mutagenesis Advance Access published online on March 27, 2006
Mutagenesis, doi:10.1093/mutage/gel015
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© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received December 20, 2005
Revised February 19, 2006
Accepted February 28, 2006

Original article

No evidence of chromosome damage in chronic obstructive pulmonary disease (COPD)

Marta Casella 1, Massimo Miniati 2, Simonetta Monti 2, Fabrizio Minichilli 3, Fabrizio Bianchi 3, and Silvana Simi 1 *

1 Cell Biology and Cytogenetics Unit, Institute of Clinical Physiology, National Research Council, Pisa, Italy
2 Pulmonary Unit, Institute of Clinical Physiology, National Research Council, Pisa, Italy
3 Epidemiology Unit, Institute of Clinical Physiology, National Research Council, Pisa, Italy

* To whom correspondence should be addressed.
Silvana Simi, E-mail: s.simi{at}ifc.cnr.it


  Abstract

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality in industrialized countries. It is characterized by a progressive airflow limitation resulting from an abnormal inflammatory response of the lungs to inhaled gases and particles. Since oxidative stress is thought to play a role in COPD, and since increased oxidative stress is associated with chromosomal instability in several diseases, we investigated whether such relationship also exists in COPD. Whole blood lymphocytes from 49 COPD patients and 48 age- and sex-matched controls were cultivated in vitro and cytogenetic damage was evaluated by micronucleus (MN) and sister-chromatid-exchange (SCE) assays. In patients with COPD, MN frequency was not significantly different from that of controls. Similarly, SCE frequency did not differ in the two groups suggesting no disturbance in DNA replication. Unlike other diseases characterized by oxidative stress, COPD does not appear to be associated with DNA damage.


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