RESUMO
BACKGROUND: Oxidative stress occurs when imbalances exist between the production of oxygen free radicals and endogenous antioxidants that neutralize their harmful effects, causing irreversible tissue damage. Oxygen free radicals readily interact with DNA, proteins, and lipids, instigating conformational changes to cellular structures and leading to derangement and dysfunction. Oxidative stress is a key feature in the pathology of COPD. As disease progression occurs, supplemental oxygen is often warranted to ameliorate dyspnea. It has been established that supplemental oxygen at > 0.60 FIO2 is an instigator of oxidative stress. We sought to determine whether chronic exposure to low-flow domiciliary oxygen served as a mechanism of ongoing oxidative stress in this patient population. This study serves to inform best practices for low-flow domiciliary oxygen therapy. METHODS: We utilized prospective data collection for this study. The exhaled-breath condensate (EBC) of 52 subjects with COPD (FEV1 < 70% of predicted normal for age and gender, height, weight, and smoking history) was evaluated for isofuran (IsoF), an oxidative stress biomarker synthesized in response to elevated tissue oxygen tension. The active control group (n = 26) was compared to the active treatment group receiving low-flow domiciliary oxygen for ≥ 6 h/d (n = 26). RESULTS: The active control group generated a mean ± SD EBC IsoF level of 35.81 ± 25.0 pg/mL compared to the active treatment group's level of 51.37 ± 42.2 pg/mL (P = .057). CONCLUSIONS: In subjects diagnosed with advanced COPD, chronic exposure to supplemental oxygen therapy at concentrations ≤ 36% did not appear to induce oxidative stress based on EBC IsoF levels. Our findings do not substantiate that chronic exposure to supplemental oxygen at concentrations < 36% instigates oxidative stress, and, therefore, changes to current domiciliary oxygen therapy prescription practices are not warranted.
