Cited by 774Antioxidant Activity and Oxidative StressChronic Obstructive Pulmonary Disease (COPD) ResearchAsthma and respiratory diseases

Systemic oxidative stress in asthma, COPD, and smokers

Rahman, I, Morrison, D, Donaldson, K, MacNee, W·1996·American Journal of Respiratory and Critical Care Medicine

Abstract

An imbalance between oxidants and antioxidants is proposed in smokers and in patients with airways diseases. We tested this hypothesis by measuring the Trolox equivalent antioxidant capacity (TEAC) of plasma and the levels of products of lipid peroxidation as indices of overall oxidative stress. The plasma TEAC was markedly reduced (0.66 +/- 0.07 mmol/L; mean +/- SEM; n = 11), with increased levels of lipid peroxidation products, in healthy chronic smokers as compared with healthy nonsmokers (1.31 +/- 0.10 mmol/L, n = 14, p < 0.001), an effect that was exaggerated in those who had smoked 1 h before the study. Plasma TEAC was also low in patients presenting with acute exacerbations of chronic obstructive pulmonary disease (COPD) (0.46 +/- 0.10 mmol/L, n = 20, p < 0.001) or asthma (0.61 +/- 0.05 mmol/L, n = 9, p < 0.01) with increases in plasma lipid peroxidation products. There was a negative correlation between superoxide anion release by stimulated neutrophils and plasma antioxidant capacity (r = -0.73, p < 0.001) in patients with acute exacerbations of COPD. The profound decrease in TEAC was associated with a decreased plasma protein sulfhydryl concentrations in acute exacerbations of COPD but not in smokers or in asthmatic subjects. Therefore smoking, acute exacerbations of COPD, and asthma are associated with a marked oxidant/antioxidant imbalance in the blood, associated with evidence of increased oxidative stress. The decreased antioxidant capacity in plasma may result from different mechanisms in these conditions.

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Crossref · 10.1164/ajrccm.154.4.8887607

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  • Subjects who develop COPD may have weakened antioxidant defenses.

    “Subjects who develop COPD, an important cause of respiratory mortality, may have weakened antioxidant defenses (Rahman et al. 1996), and PM2.5 can produce oxidative stress, in part because of lung inflammation (Dagher et al. 2005; Zeka et al. 2006).”

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Authors
Rahman, I., Morrison, D., Donaldson, K., & MacNee, W.
Affiliations
Edinburgh Royal Infirmary (GB)
Venue
American Journal of Respiratory and Critical Care Medicine
Published
1996-10-01
Volume
154
Issue
4
Pages
1055-1060
ISSN
  • 1073-449X (ISSN-L)
  • 1535-4970
OpenAlex
W1984454286
Cited by
774
References
30
Citations by year
2026: 1 · 2025: 9 · 2024: 9 · 2023: 13 · 2022: 15 · 2021: 16 · 2020: 23 · 2019: 18 · 2018: 16 · 2017: 24 · 2016: 20 · 2015: 28 · 2014: 27 · 2013: 25 · 2012: 33
FWCI
12.55
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Respiratory and Critical Care Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
Keywords
oxidative stress, asthma, chronic obstructive pulmonary disease, COPD exacerbations, smoking, plasma antioxidant capacity, lipid peroxidation, superoxide, neutrophils, protein sulfhydryl groups, oxidant-antioxidant imbalance
MeSH terms
Adult, Aged, Asthma, Female, Humans, Lipid Peroxides, Lung Diseases, Obstructive, Male, Middle Aged, Smoking, Sulfhydryl Compounds, Superoxides, Lipid Peroxidation, Case-Control Studies, Oxidative Stress

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