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

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.