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

Abstract

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; <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>15</mml:mn></mml:mrow></mml:math>); group of nonphysical exercise (COPD; <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mrow><mml:mi>n</mml:mi><mml:mo>=</mml:mo><mml:mn>36</mml:mn></mml:mrow></mml:math>)) 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.