Although an oxidants and antioxidants imbalane has been considered in the pathogenesis of chronic obstructive pulmonary disease (COPD), there is a paucity of reports focussing on the smoking-induced changes of oxidants and antioxidants in COPD.

The concentration of antioxidants (ascorbic acid, uric acid, retinol, and α- & γ-tocopherol) was measured in the serum and induced sputum of 30 healthy controls and 34 stable COPD patients using high performance liquid chromatography (HPLC). The inhibition of lipid peroxidation as an index of antioxidant capacity was measured in the serum by a TBA assay.

The serum concentration of ascorbic acid, α-tocopherol, and retinol were significantly lower in the patients with COPD than in healthy controls (484.8±473.3 vs 1497.8±819.2 pmol/L, p<0.001, 48.38±17.34 vs 73.96±26.29 pmol/L, p<0.001, and 9.51±8.33 vs 15.01±5.88 pmol/L, p<0.05, respectively, mean±SD). However, there were little differences in the ascorbic acid and uric acid concentrations in the induced sputum between the COPD patients and the controls. The induced sputum to serum ratio of ascorbic acid was significantly higher in COPD patients compared with healthy control (0.375 vs 0.085, p<0.05). In the normal controls, the serum ascorbic acid concentration was lower in smokers than in nonsmokers (1073±536 vs 1757±845 pmol/L, p<0.05), but the level was still higher than that of the COPD patients (p<0.05). The serum retinol levels were correlated with FEV1 in COPD patients (r=0.58, p<0.05). The products of lipid peroxidation were increased in normal smokers and COPD compared with normal nonsmokers (115.56±19.93 and 120.02±24.56 vs 91.87±20.71 µmol/µmol Pi of liposome, p<0.05).

Cigarette smoking may induce the depletion of serum antioxidants and this depletion of antioxidants is suggested to play a role in the pathogenesis of COPD.