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Activated polymorphonuclear leucocytes consume vitamin C.

H Hemilä, P Roberts, M Wikström

    FEBS Letters
    |December 3, 1984
    PubMed
    Summary
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    Activated human immune cells, polymorphonuclear leucocytes (PMN), oxidize extracellular ascorbate. This process, driven by superoxide and myeloperoxidase, suggests ascorbate protects against inflammation-related oxygen radical damage.

    Area of Science:

    • Biochemistry
    • Immunology
    • Cell Biology

    Background:

    • Polymorphonuclear leucocytes (PMN) are key immune cells.
    • Activated PMN produce superoxide and other oxygen derivatives for microbial defense.
    • The role of extracellular ascorbate in PMN-mediated oxidative processes is not fully understood.

    Purpose of the Study:

    • To investigate the interaction between extracellular ascorbate and activated human PMN.
    • To determine the mechanisms by which PMN affect ascorbate in vitro.
    • To assess the potential protective role of ascorbate against PMN-induced oxidative damage.

    Main Methods:

    • In vitro incubation of human PMN with extracellular ascorbate.
    • Measurement of ascorbate oxidation.

    Related Experiment Videos

  • Enzymatic assays using superoxide dismutase.
  • Quantification of oxygen consumption and stoichiometry.

    • Main Results:

    • Activated human PMN effectively oxidize extracellular ascorbate, while resting PMN do not.
    • Superoxide generated by activated PMN is the primary driver of ascorbate oxidation, as evidenced by inhibition with superoxide dismutase.
    • Myeloperoxidase also contributes significantly to ascorbate oxidation.
    • Ascorbate reduces superoxide to peroxide, consistent with stoichiometric measurements.

    Conclusions:

    • Extracellular ascorbate is readily oxidized by activated human PMN.
    • The oxidation is primarily mediated by superoxide and, to a lesser extent, by myeloperoxidase.
    • Ascorbate's ability to reduce superoxide suggests it acts as a physiological antioxidant, protecting against oxygen radical damage during inflammation.