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Related Experiment Videos

Nitric oxide synthase inhibitors decrease human polymorphonuclear leukocyte luminol-dependent chemiluminescence

S D Catz1, M C Carreras, J J Poderoso

  • 1Laboratory of Oxygen Metabolism, University Hospital, University of Buenos Aires, Argentina.

Free Radical Biology & Medicine
|December 1, 1995
PubMed
Summary
This summary is machine-generated.

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Nitric oxide synthase (NOS) pathway products are essential for optimal luminol chemiluminescence (CL) in human neutrophils. This suggests peroxynitrite (ONOO-) may be an unrecognized mediator in this light-emitting reaction.

Area of Science:

  • Immunology
  • Biochemistry
  • Cellular Physiology

Background:

  • Nitric oxide synthase (NOS) inhibitors modulate luminol-dependent chemiluminescence (CL) in macrophages.
  • Peroxynitrite (ONOO-), a potent oxidant, can directly react with luminol to produce CL in cell-free systems.

Purpose of the Study:

  • To investigate the role of the L-arginine/NOS pathway in luminol CL.
  • To evaluate the impact of NOS inhibitors on human polymorphonuclear (PMN) leukocytes' luminol CL.
  • To determine the involvement of nitric oxide (NO) and superoxide anion (O2.-) production in this process.

Main Methods:

  • Utilized NG-monomethyl-L-arginine (L-NMMA) and N-iminoethyl-L-ornithine (L-NIO) as NOS inhibitors.
  • Measured nitric oxide (NO) release via oxymyoglobin oxidation.

Related Experiment Videos

  • Assessed superoxide anion (O2.-) production and luminol CL in phorbol ester-activated human PMNs.

    • Main Results:

    • Luminol CL was dose-dependently diminished by L-NMMA.
    • Superoxide dismutase (SOD) reduced luminol CL, an effect potentiated by L-NMMA.
    • L-NMMA significantly decreased both NO and O2.- production; L-NIO attenuated CL but not O2.- production.

    Conclusions:

    • Maximal luminol CL in human PMNs requires products from both NOS and NADPH oxidase catalytic activity.
    • The NOS pathway is integral to luminol CL in human PMNs.
    • Peroxynitrite (ONOO-) is proposed as a potential, unrecognized mediator in this chemiluminescence phenomenon.