DNA Damage and Oxidative Stress in Patients with Chronic Obstructive Pulmonary Disease



Andréa Lúcia G da Silvaa, b, *, Helen T da Rosac, Clara F Charlierb, Miriam Salvadord, Dinara J Mourae, f, Andreia R de Moura Valime, Temenouga N Guechevab, g, João Antônio Pegas Henriquesb, d, g
a Department of Health and Physical Education, University of Santa Cruz do Sul - UNISC, Santa Cruz do Sul/RS, Brazil
b Cellular and Molecular Biology Program, Federal University of Rio Grande do Sul - UFRGS, Porto Alegre/RS, Brazil
c Scientific Initiation of University of Santa Cruz do Sul - UNISC, Santa Cruz do Sul/RS, Brazil
d Institute of Biotechnology, University of Caxias do Sul, Caxias do Sul/RS, Brazil
e Department of Biology and Pharmacy, University of Santa Cruz do Sul - UNISC, Santa Cruz do Sul/RS, Brazil
f Laboratory of Genetic Toxicology – Federal University of Health Sciences of Porto Alegre - UFCSPA, Porto Alegre/RS, Brazil
g Department of Biophysics, Federal University of Rio Grande do Sul-UFRGS, Porto Alegre/RS, Brazil


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© 2013 da Silva et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Avenida Independência, 2293, Bloco 42, Bairro Universitário, Santa Cruz do Sul/RS- Brasil; Tel: +55 51 37177374; Fax: +55 51 37171855; E-mail: andreag@unisc.br


Abstract

Background:

We aimed to assess the level of DNA damage and susceptibility to exogenous mutagens in peripheral blood cells of Chronic Obstructive Pulmonary Disease (COPD) patients and healthy individuals by comet assay. Oxidative stress was also evaluated by means of thiobarbituric acid reactive species (TBARS) in blood plasma.

Methods:

Case-control study enrolling 51 COPD patients and 51 controls. Peripheral blood was used to perform the alkaline (pH>13) and neutral (pH=8.5) comet assay. For the assessment of susceptibility to exogenous DNA damage, the cells were treated with methylmethane sulfonate (MMS) for 1-hour or 3-hour at 37° C. The percentage of residual DNA damage after 3-h MMS treatment was calculated using the value of 1-h MMS treatment for each subject as 100%. Lipid peroxidation was evaluated by measuring TBARS in blood plasma.

Results:

DNA damage in patients was significantly higher than in controls as measured by the neutral and alkaline comet assay. Residual DNA damage detected after MMS treatment increased in patients, in contrast to controls, indicating higher susceptibility to alkylation damage and/or repair inhibition. High susceptibility to exogenous DNA damage in COPD patients correlates with high amount of TBARS and low forced vital capacity and expiratory volume.

Conclusion:

The positive correlation between increased susceptibility to exogenous DNA damage and TBARS levels in COPD patients suggests the possible involvement of oxidative stress in damage induction and/or repair inhibition.

Keywords: COPD, DNA damage, repair, comet assay, lipid peroxidation.