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a Respiratory Medicine
Unit, Royal Infirmary, Edinburgh, UK, b Department of Medicine and
Therapeutics, University College Dublin, Ireland, c Department of Pulmonology, Leiden University
Medical Centre, Leiden, The Netherlands
Correspondence to: Professor W MacNee, ELEGI Colt Research Laboratories, Wilkie Building, Medical School, University of Edinburgh, Edinburgh EH8 9AG, UK
Received 2 March 1999; Returned to authors 4 June 1999; Revised version received 7 December 1999; Accepted for publication 8 December 1999
BACKGROUND
It has been
suggested that oxidative stress is an important factor in the
pathogenesis of chronic obstructive pulmonary disease (COPD). We have
shown that an oxidant/antioxidant imbalance occurs in the distal air
spaces of smokers and in patients with COPD which is reflected
systemically in the plasma. A study was undertaken to determine whether
plasma antioxidant status correlated with lung function as assessed by
forced expiratory volume in one second (FEV1) and forced
vital capacity (FVC) in smokers and patients with COPD.
METHODS
Plasma
antioxidant capacity, assessed by the Trolox equivalent antioxidant
capacity (TEAC) as an index of overall systemic oxidative stress, and
protein thiol levels were measured in 95 patients with stable COPD, in
82 healthy smokers, and in 37 healthy non-smokers.
RESULTS
Mean (SE)
plasma TEAC levels were significantly decreased in patients with COPD
(0.81 (0.03) mmol/l, p<0.001) and in healthy smokers (0.87 (0.04) mmol/l, p<0.001) compared with healthy non-smokers (1.31 (0.11) mmol/l). The mean differences in plasma antioxidant capacity
(mM) were (0.81, 95% confidence interval (CI) 0.22 to 1.48), (0.87, 95% CI 0.2 to 1.46), and (1.31, 95% CI 1.09 to 1.58) in patients with
COPD, healthy smokers, and healthy non-smokers, respectively. This
reduction was associated with a 29% (95% CI 18 to 38) and a 30%
(95% CI 19 to 40) decrease in plasma protein thiol levels in COPD
patients and smokers, respectively. Current smoking was not the main
contributor to the reduction in antioxidant capacity in patients with
COPD as those patients who were still smokers had similar TEAC levels
(mean (SE) 0.78 (0.05); n = 25) to those who had stopped smoking (0.84 (0.02); n = 70). No significant correlations were found between
spirometric data measured as FEV1 % predicted or
FEV1/FVC % predicted and the plasma levels of TEAC in
patients with COPD, healthy smokers, or healthy non-smokers. Similarly,
there was no significant correlation between FEV1 % predicted or FEV1/FVC % predicted and the levels of plasma
protein thiols in the three groups.
CONCLUSIONS
These data
confirm decreased antioxidant capacity in smokers and patients with
COPD, indicating the presence of systemic oxidative stress. However, no
relationship was found between protein thiols or TEAC levels and
measurements of airflow limitation in either smokers or in patients
with COPD.
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