Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar macrophages.
Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leucocytes (PMN) and alveolar marcophages (AM) obtained from guinea-pigs exposed to 85% oxygen for 90 h. The influence of these altered enzyme activities on the rate of oxygen consumption and release of superoxide anion (O--2) and hydrogen peroxide (H2O2) was investigated. By 18 h O--2 released from resting PMN increased two-fold and remained elevated through the entire periods of the study, whereas H2O2 release and oxygen consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of O--2 and H2O2 and consumed significantly more oxygen compared to the usual increase noted at earlier time points. Although oxygen consumption was almost two-fold higher in AM than PMN, phagocytizing AM released three-fold less O--2 and five-fold less H2O2 than did PMN. Furthermore, AM of animals exposed to hyperoxia no longer exhibited enhanced O--2 production upon exposure to opsonized zymosan. Hydrogen peroxide release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in oxygen 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.
D000818:Animals; D006168:Guinea Pigs; D006861:Hydrogen Peroxide / Q000378:metabolism*; D066298:In Vitro Techniques; D008264:Macrophages / Q000378:metabolism*; D009504:Neutrophils / Q000378:metabolism*; D010100:Oxygen; D010101:Oxygen Consumption; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000166:cytology; D013481:Superoxides / Q000378:metabolism
D013481:Superoxides; D006861:Hydrogen Peroxide; D010100:Oxygen