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Inhalation Toxicology
International Forum for Respiratory Research
Volume 22, 2010 - Issue 10
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Research Article

Malondialdehyde and superoxide dismutase correlate with FEV1 in patients with COPD associated with wood smoke exposure and tobacco smoking

, , , , , & show all
Pages 868-874 | Received 13 Nov 2009, Accepted 02 May 2010, Published online: 28 Jun 2010
 

Abstract

Tobacco smoking is the primary risk factor for chronic obstructive pulmonary disease (COPD). However, recent epidemiological studies have established domestic exposure to wood smoke and other biomass fuels as additional important risk factors, characteristic in developing countries. Oxidative stress is one of the mechanisms concerned with pathogenesis of COPD. However, the molecular mechanisms involved in the onset and progress of COPD associated with biomass and specifically that derived from wood smoke exposure remain unknown. We analyzed the relationship between forced expiratory volume in first second (FEV1) with plasma malondialdehyde (MDA) concentration and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) in COPD patients associated with wood smoke (WSG; n = 30), tobacco smoking (TSG; n = 30), and healthy control subjects (HCG; n = 30). Differences between FEV1 from WSG and TSG (58 ± 22% and 51 ± 24%, respectively) with HCG (100 ± 6%) were observed (P < 0.01). Plasma MDA concentration was higher in both WSG and TSG (1.87 ± 0.81 and 1.68 ± 0.82 nmol/mL, respectively) compared with HCG (0.42 ± 0.17 nmol/mL; P < 0.01). SOD activity showed a significant increase in both WSG and TSG (0.36 ± 0.12 and 0.37 ± 0.13 U/mL) compared with HCG (0.19 ± 0.04 U/mL; P < 0.01). No differences were shown regarding GPx, GR, and GST activities between COPD and control groups. Inverse correlations were founded between MDA and SOD with FEV1 in both COPD patients and control subjects (P < 0.001). These results indicate a role for oxidative stress in COPD associated with wood smoke similar to that observed with tobacco smoking in subjects who ceased at least 10 years previous to this study.

Acknowledgements

Declaration of interest

This work was supported and financed by a grant from the Consejo Nacional de Ciencia y Tecnología (CONACYT) México, project number III-90942. Institution where the work was performed: Instituto Nacional de Enfermedades Respiratorias “Ismael Cosío Villegas” (INER). The authors declare that there are no conflicts of interest related to the article or the research described.

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