Hydrogen peroxide production by alveolar macrophages is increased and its concentration is elevated in the breath of rats exposed to hypoxia:relationship to lung lipid peroxidation
Abstrakt
Hypoxic exposure triggers a generation of reactive oxygen species that initiate free radical damage to the lung. Hydrogen peroxide is the product of alveolar macrophages detectable in the expired breath.
We evaluated the significance of breath H2O2 concentration for the assessment of lung damage after hypoxic exposure and during posthypoxic period. Adult male rats were exposed to normobaric hypoxia (10% O-2) for 3 hours or 5 days.
Immediately after the hypoxic exposure and then after 7 days or 14 days of air breathing, H2O2 was determined in the breath condensate and in isolated lung macrophages. Lipid peroxidation was measured in lung homogenates.
Three-hour hypoxia did not cause immediate increase in the breath H2O2; 5-day hypoxia increased breath H2O2 level to 458%. After 7 days of subsequent air breathing H2O2 was elevated in both groups exposed to hypoxia.
Increased production of H2O2 by macrophages was observed after 5 days of hypoxia and during the 7 days of subsequent air breathing. Lipid peroxidation increased in the periods of enhanced H2O2 generation by macrophages.
As the major increase (1040%) in the breath H2O2 concentration found 7 days after 3 hours of hypoxia was not accompanied by lipid peroxidation, it can be concluded that the breath H2O2 is not a reliable indicator of lung oxidative damage.