Objective: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by recurrent hypoxia/reoxygenation during sleep that may cause oxidative stress. The aim of the study was to explore whether obstructive sleep apnea-hypopnea syndrome could induce higher production of hydrogen peroxide in exhaled breath condensate (EBC).
Methods: Thirty-two patients with OSAHS (18 smokers and 14 non-smokers) and 10 age matched controls were enrolled in the study. EBC was collected before and after sleep at the same night from both groups. H2O2 was tested in EBC fluorimetrically.
Results: There was no difference of pre-sleep H2O2 level among OSAHS smoker group, OSAHS non-smoker group and the control subjects [(0.88 +/- 0.36) micromol/L, (0.87 +/- 0.45) micromol/L and (0.86 +/- 0.46) micromol/L, F = 0.01, P = 0.99]. There was a significantly increased level of H2O2 after sleep for both smoking or no-smoking OSAHS patients [post-sleep: smoker: (1.65 +/- 0.89) micromol/L, t = 3.43, P = 0.001; non smoker: (1.82 +/- 1.12) micromol/L, t = 2.95, 0.007]. The control group did not show such a change [post-sleep: (0.71 +/- 0.36) micromol/L, t = 0.81, P = 0.43]. OSAHS group, either smokers or non-smokers, showed a significantly higher post-sleep H2O2 level in EBC compared with that of controls (F = 5.11, P = 0.01). Post-sleep H2O2 level (beta = -0.36, P = 0.02) and the variation of H2O2 level (beta = -0.38, P = 0.01) correlated negatively with the minimal SpO2 during sleep period.
Conclusions: Oxidative stress of respiratory tract is a characteristic change in OSAHS. Nocturnal hypoxia may be related to these changes, which may be involved in the lung injury of OSAHS.