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No evidence of chromosome damage in chronic obstructive pulmonary disease (COPD)
Author(s) -
Marta Casella,
Massimo Miniati,
Simonetta Monti,
Fabrizio Minichilli,
Fabrizio Bianchi,
Silvana Simi
Publication year - 2006
Publication title -
mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.723
H-Index - 91
eISSN - 1464-3804
pISSN - 0267-8357
DOI - 10.1093/mutage/gel015
Subject(s) - copd , oxidative stress , sister chromatid exchange , dna damage , medicine , micronucleus test , micronucleus , pulmonary disease , chromosome instability , immunology , sister chromatids , lymphocyte , genome instability , chromosome , pathology , biology , dna , genetics , gene , toxicity
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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