Literature DB >> 20583895

Malondialdehyde and superoxide dismutase correlate with FEV(1) in patients with COPD associated with wood smoke exposure and tobacco smoking.

Martha Montaño1, José Cisneros, Alejandra Ramírez-Venegas, José Pedraza-Chaverri, Daniel Mercado, Carlos Ramos, Raul H Sansores.   

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 (FEV(1)) 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 FEV(1) 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 FEV(1) 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.

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Year:  2010        PMID: 20583895     DOI: 10.3109/08958378.2010.491840

Source DB:  PubMed          Journal:  Inhal Toxicol        ISSN: 0895-8378            Impact factor:   2.724


  23 in total

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Review 3.  Clinical Characteristics of Patients With Biomass Smoke-Associated COPD and Chronic Bronchitis, 2004-2014.

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Review 4.  Indoor Air Pollution and Respiratory Health.

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6.  Correlation of apical fluid-regulating channel proteins with lung function in human COPD lungs.

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8.  SUL-151 Decreases Airway Neutrophilia as a Prophylactic and Therapeutic Treatment in Mice after Cigarette Smoke Exposure.

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Review 10.  A Systematic Review of Innate Immunomodulatory Effects of Household Air Pollution Secondary to the Burning of Biomass Fuels.

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