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American Journal of Respiratory and Critical Care Medicine Vol 166. pp. S4-S8, (2002)
© 2002 American Thoracic Society

Article

Reactive Oxygen Species and Cell Signaling

Respiratory Burst in Macrophage Signaling

Henry Jay Forman and Martine Torres

Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama; and Department of Pediatrics, Children's Hospital Los Angeles Research Institute, Keck School of Medicine, University of Southern California, Los Angeles, California

Correspondence and requests for reprints should be addressed to Henry Jay Forman, Ph.D., Department of Environmental Health Sciences, School of Public Health, 1530 3rd Avenue S, RPHB 317, University of Alabama at Birmingham, Birmingham, AL 35294. E-mail: hforman{at}uab.edu

ABSTRACT

Phagocytes such as neutrophils and macrophages produce reactive oxygen species (ROS) during phagocytosis or stimulation with a wide variety of agents through activation of nicotinamide adenine dinucleotide phosphate reduced (NADPH) oxidase that is assembled at the plasma membrane from resident plasma membrane and cytosolic protein components. One of the subunits of the phagocyte NADPH oxidase is now recognized as a member of a family of NADPH oxidases, or NOX, present in cells other than phagocytes. Physiologic generation of ROS has been implicated in a variety of physiologic responses from transcriptional activation to cell proliferation and apoptosis. The increase in superoxide and hydrogen peroxide (H2O2) that results from stimulation of the NADPH oxidase is transient, in part due to the presence of the antioxidant enzymes, which return their concentrations to the prestimulation steady state level. Thus, the antioxidant enzymes may function in the "turn-off" phase of signal transduction by ROS. During its transient elevation, H2O2 may act as a modifier of key signaling enzymes through reversible oxidation of critical thiols. The rapid reaction of thiols with H2O2 when in their unprotonated state would provide a potential mechanism for the specificity that is necessary for physiologic cell signaling.

Key Words: protein tyrosine phosphatase • mitogen-activated kinase • transcription factors • superoxide • hydrogen peroxide




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