Effect of Hyperoxia on Superoxide Anion and Hydrogen Peroxide Production of Polymorphonuclear Leucocytes and Alveolar Macrophages

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Abstract
Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leukocytes (PMN) and alveolar macrophages (AM) obtained from guinea-pigs exposed to 85% O2 for 90 h. The influence of these altered enzyme activities on the rate of O2 consumption and release of superoxide anion .**GRAPHIC**. and H2O2 was investigated. By 18 h .**GRAPHIC**. released from resting PMN increased 2-fold and remained elevated through the entire period of the study, but H2O2 release and O2 consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of .**GRAPHIC**. and H2O2 and consumed significantly more O2 compared to the usual increase noted at earlier time points. Although O2 consumption was almost 2-fold higher in AM than PMN, phagocytizing AM released 3-fold less .**GRAPHIC**. and 5-fold less H2O2 than did PMN. AM of animals exposed to hyperoxia no longer exhibited enhanced .**GRAPHIC**. production upon exposure to opsonized zymosan. H2O2 release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in O2 consumption of AM occurred during hyperoxia. The divergent oxidative responses in PMN and AM of guinea-pigs exposed to hyperoxia suggest different biochemical adaptive mechanisms.