Table of Contents
ISRN Pulmonology
Volume 2013, Article ID 907520, 8 pages
Research Article

Effect of Physical Exercise on the Level of DNA Damage in Chronic Obstructive Pulmonary Disease Patients

1Department of Health and Physical Education, University of Santa Cruz do Sul (UNISC), Avenida Independência 2293, Bloco 42, Bairro Universitário, Santa Cruz do Sul, RS, Brazil
2Cellular and Molecular Biology Program, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil
3Fellowship of Scientific Initiation, University of Santa Cruz do Sul (UNISC), Santa Cruz do Sul, RS, Brazil
4Institute of Biotechnology, University of Caxias do Sul, Caxias do Sul, RS, Brazil
5Department of Biology and Pharmacy, University of Santa Cruz do Sul (UNISC), Santa Cruz do Sul, RS, Brazil
6Laboratory of Genetic Toxicology, Federal University of Health Sciences of Porto Alegre (UFCSPA), Porto Alegre, RS, Brazil
7Department of Biophysics, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil

Received 26 November 2012; Accepted 4 January 2013

Academic Editors: A. M. Boylan and Y. Dobashi

Copyright © 2013 Andréa Lúcia G. da Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study assessed the chronic effects of physical exercise on the level of DNA damage and the susceptibility to exogenous mutagens in peripheral blood cells of chronic obstructive pulmonary disease (COPD) patients. The case-control study enrolled COPD patients separated into two groups (group of physical exercise (PE-COPD; ); group of nonphysical exercise (COPD; )) and 51 controls. Peripheral blood was used to evaluate DNA damage by comet assay and lipid peroxidation by measurement of thiobarbituric acid reactive species (TBARS). The cytogenetic damage was evaluated by the buccal micronucleus cytome assay. The results showed that the TBARS values were significantly lower in PE-COPD than in COPD group. The residual DNA damage (induced by methyl methanesulphonate alkylating agent) in PE-COPD was similar to the controls group, in contrast to COPD group where it was significantly elevated. COPD group showed elevated frequency of nuclear buds (BUD) and condensed chromatin (CC) in relation to PE-COPD and control groups, which could indicate a deficiency in DNA repair and early apoptosis of the damaged cells. We concluded that the physical exercise for COPD patients leads to significant decrease of lipid peroxidation in blood plasma, decrease of susceptibility to exogenous mutagenic, and better efficiency in DNA repair.