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Oxidants Formed by the Respiratory Burst

Their Physiological Role and Their Involvement in the Oxidative Metabolism and Activation of Drugs, Carcinogens, and Xenobiotics

  • Chapter
The Respiratory Burst and Its Physiological Significance

Abstract

Phagocytic neutrophils exhibit a burst in oxygen consumption that is cyanide resistant—the respiratory burst—when the cells are exposed to various soluble stimuli (e.g., chemotactic oligopeptides, complement fragments) or particulate stimuli (e.g., opsonized bacteria).1 The respiratory response involves a recognition site on the plasma membrane surface that leads to the release of an intracellular signal.1 Transduction of this signal causes the activation of a plasma membrane NADPH oxidase that we suggested was responsible for the respiratory burst,2 and that was confirmed by others.1 The superoxide anion O -2 · formed is released outside the cell, where it dismutates into H2O2. H2O2 may also diffuse back into the neutrophil, where it is decomposed by intracellular myeloperoxidase, GSH/GSH-peroxidase and catalase. When particulate stimuli are completely engulfed within a phagocytic vacuole, superoxide and the dismutation product H2O2 accumulate in the vacuole and diffuse into the cytoplasm.

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© 1988 Plenum Press, New York

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O’Brien, P.J. (1988). Oxidants Formed by the Respiratory Burst. In: Sbarra, A.J., Strauss, R.R. (eds) The Respiratory Burst and Its Physiological Significance. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5496-3_10

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  • DOI: https://doi.org/10.1007/978-1-4684-5496-3_10

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