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The Biology and Pathology of Oxygen Radicals

JOE M. McCORD, Ph.D.; and IRWIN FRIDOVICH, Ph.D.
[+] Article and Author Information

▸Requests for reprints should be addressed to Irwin Fridovich, Ph.D.; Department of Biochemistry, Duke University Medical Center; Durham, NC 27710.


Mobile, Alabama, and Durham, North Carolina A New York University Honors Program Lecture


© 1978 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1978;89(1):122-127. doi:10.7326/0003-4819-89-1-122
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Superoxide radicals (O2-) are commonplace products of the biological reduction of oxygen. Their intrinsic reactivity and ability to generate other more reactive entities constitute a threat to cellular integrity. Superoxide dismutases, enzymes that catalytically scavenge these radicals, have evolved to meet this threat. These metalloenzymes are essential for respiring organisms to survive. Several compounds, such as the antibiotic streptonigrin and the herbicide paraquat, augment the production rate of O2- inside cells. This accounts for the oxygen-enhancement of their lethality. Some bacteria respond to this artificially increased rate of O2- production by synthesizing additional superoxide dismutase. Ionizing radiation generates O2- in its passage through oxygenated aqueous media, and superoxide dismutase, added to the suspending medium, decreases the oxygen-enhancement of the lethality of such irradiation of the bacterium Escherichia coli. Production of O2- by activated neutrophils is clinically significant, since it is an important component of the bactericidal actions of these cells and the inflammatory process. Superoxide dismutases exert an anti-inflammatory action that may be useful in managing inflammations.

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