%0 Journal Article
%T Effect of Physical Exercise on the Level of DNA Damage in Chronic Obstructive Pulmonary Disease Patients
%A Andr¨¦a L¨˛cia G. da Silva
%A Helen T. da Rosa
%A Eduarda Bender
%A Paulo Ricardo da Rosa
%A Mirian Salvador
%A Clara F. Charlier
%A Dinara Jaqueline Moura
%A Andr¨¦ia R. de Moura Valim
%A Temenouga N. Guecheva
%A JoŁżo AntŁżnio Pegas Henriques
%J ISRN Pulmonology
%D 2013
%R 10.1155/2013/907520
%X 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. 1. Introduction The chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality in countries with different levels of economic development, and it is estimated that in 2020 the COPD will become the third leading cause of death all over the world [1, 2]. COPD is currently defined as a preventable and treatable disease characterized by airflow limitation, resulting from an abnormal inflammatory reaction to inhaled particles from cigarette smoking and associated with comorbidities [2]. The COPD is multifactorial and its pathology often includes systemic inflammation and oxidative stress [3, 4]. The formation of reactive oxygen species (ROS) by cigarette smoke and inflammatory cells, generated in the pulmonary epithelium, has been associated with slowly progressive and irreversible decrease in forced expiratory volume in one second (FEV1), loss of muscle mass, and muscle dysfunction [3, 4, 11] and probably modulates some of the systemic effects of COPD (i.e., skeletal muscles atrophy, osteoporosis, anemia, and cachexia [11, 12]). Some of the many different compounds in cigarette smoke can react directly with cellular components to form ROS while other carcinogens must be activated to produce single- and double-strand
%U http://www.hindawi.com/journals/isrn.pulmonology/2013/907520/