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Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar

M Rister, R L Baehner

    British Journal of Haematology
    |June 1, 1977
    PubMed

    Insights

    Hyperoxia alters antioxidant enzymes in immune cells. Polymorphonuclear leucocytes (PMN) and alveolar macrophages (AM) show distinct responses to prolonged oxygen exposure, suggesting varied adaptive mechanisms.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Physiology

    Background:

    • Hyperoxia, or elevated oxygen levels, can induce oxidative stress.
    • Antioxidant enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase play crucial roles in cellular defense against reactive oxygen species.
    • Polymorphonuclear leucocytes (PMN) and alveolar macrophages (AM) are key immune cells involved in inflammatory responses and host defense.

    Purpose of the Study:

    • To investigate the impact of prolonged hyperoxia on antioxidant enzyme activities in guinea-pig PMN and AM.
    • To determine how altered enzyme activities influence oxygen consumption and the release of superoxide anion (O2-) and hydrogen peroxide (H2O2).
    • To explore the divergent biochemical adaptive mechanisms in PMN and AM during hyperoxia.

    Main Methods:

    • Guinea-pigs were exposed to 85% oxygen for 90 hours.
    • Activities of SOD, catalase, and glutathione peroxidase were measured in PMN and AM.
    • Oxygen consumption, O2- release, and H2O2 release were assessed in resting and phagocytizing cells (opsonized zymosan).

    Main Results:

    • Hyperoxia activated SOD while inactivating catalase and glutathione peroxidase in both PMN and AM.
    • Resting PMN showed a two-fold increase in O2- release by 18 hours, with no change in H2O2 release or oxygen consumption.
    • During phagocytosis, PMN exhibited increased O2-, H2O2 release, and oxygen consumption at 66 hours.
    • AM consumed more oxygen than PMN but released significantly less O2- and H2O2.
    • Hyperoxia-exposed AM lost enhanced O2- production capacity upon stimulation and showed decreased resting H2O2 release but increased release during phagocytosis, with no change in oxygen consumption.

    Conclusions:

    • Prolonged hyperoxia induces distinct enzymatic and oxidative responses in PMN and AM.
    • PMN demonstrate enhanced oxidative burst capacity under hyperoxia, particularly during phagocytosis.
    • AM exhibit a dampened oxidative response to hyperoxia, suggesting different cellular protection strategies.

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