Abstract
To test the effect of transition from sustained hypoxia to normoxia on production of reactive oxygen species (ROS) in lungs, the authors measured hydrogen peroxide (H2O2) output in the expired air of rats breathing hypoxic, normoxic, and hyperoxic gas mixtures at the end of exposure to 72 hours of hypoxia. Twenty-one male Wistar rats (200 to 280 g) were randomly assigned to 1 of 3 groups.
First two groups (experimental) were kept for 3 days in normobaric hypoxic chamber (F1O2 0.1), rats of the third group (controls) breathed air. The rats were then anesthetized, intubated, placed in the plethysmograph, and their ventilation measured.
Two periods of exhaled breath condensate (EBC) collection, each lasting 1 hour, were then performed to assay H2O2 output. The controls breathed during both samplings air, the first experimental group breathed during first sampling period hypoxic mixture (F1O2 0.1; SH-H measurement) and then, during second period, air (SH-H-A measurement), the second experimental group breathed first air (SH-A measurement) and then hyperoxic mixture (F1O2 1.0; SH-A-O-2 measurement).
Concentration of H2O2 in the EBC was assayed by chemiluminescence. H2O2 production in the control group was low and similar in both measurements (20+/-10 and 13+/-5 pmol/h, mean+/-SEM).
Exposure to 72 hours of hypoxia increased the H2O2 production to 105+/-18 pmol/h (SH-H). Transition from hypoxia to normoxia resulted in an increase in the H2O2 production (SH-A 421+/-24 pmol/h, and SH-H-A 366+/-19 pmol/h).
Following transition from air breathing to hyperoxia did not affect the H2O2 production (SH-A-O-2 373+/-25 pmol/h). The results showed that sustained hypoxia and transition from sustained hypoxia to normoxia increased H2O2 formation in the lungs.