Volume 19, Issue 1 pp. 74-79
ORIGINAL ARTICLE

Monitoring oxidative stress during chronic obstructive pulmonary disease exacerbations using malondialdehyde

Balazs Antus

Corresponding Author

Balazs Antus

Department of Pulmonology, National Koranyi Institute of TB and Pulmonology, Budapest, Hungary

Department of Pathophysiology, National Koranyi Institute of TB and Pulmonology, Budapest, Hungary

Correspondence: Balazs Antus, Department of Pathophysiology, National Koranyi Institute of TB and Pulmonology, Piheno ut 1, H-1121 Budapest, Hungary. Email: [email protected]Search for more papers by this author
Gabriella Harnasi

Gabriella Harnasi

Department of Pathology, National Koranyi Institute of TB and Pulmonology, Budapest, Hungary

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Orsolya Drozdovszky

Orsolya Drozdovszky

Department of Pathophysiology, National Koranyi Institute of TB and Pulmonology, Budapest, Hungary

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Imre Barta

Imre Barta

Department of Pulmonology, National Koranyi Institute of TB and Pulmonology, Budapest, Hungary

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First published: 08 July 2013
Citations: 58
(Associate Editor: Paul Thomas).

Abstract

Background and objective

Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). In this longitudinal study changes in the level of malondialdehyde (MDA), an end product of polyunsaturated fatty acid peroxidation, were investigated in the airways of patients with acute exacerbation of COPD (AECOPD).

Methods

Levels of MDA were measured in sputum and exhaled breath condensate (EBC) of 34 COPD patients at the time of hospital admission due to an acute exacerbation of the disease, and again following treatment at the time of hospital discharge. MDA was also assessed in 21 stable patients with COPD and 20 healthy controls. Measurements were performed using high-performance liquid chromatography.

Results

Sputum MDA levels were significantly increased in AECOPD (220.0 ± 17.5 nmol/L) compared with stable disease (144.6 ± 14.3 nmol/L, P < 0.01) and healthy controls (85.9 ± 11.3 nmol/L, P < 0.001). MDA levels decreased after treatment (190.7 ± 16.3 nmol/L, P < 0.05). In contrast to sputum, EBC MDA levels were comparable between controls, stable COPD patients and AECOPD patients (73.1 ± 5.1 nmol/L, 96.1 ± 11.6 nmol/L and 93.3 ± 7.6 nmol/L, P = NS). Measurement of MDA had good repeatability in both sputum and EBC, but the between-day variability was considerably higher in EBC. Sputum induction did not influence MDA levels.

Conclusions

MDA in sputum, but not in EBC, appears to be a useful marker for monitoring exacerbation-associated oxidative stress in AECOPD.

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