Mechanisms of cellular injury: potential sources of oxygen free radicals in ischemia/reperfusion.
Oxygen-derived free radicals have been implicated as a mediator of the microvascular and parenchymal cell injury associated with reperfusion of ischemic tissues. Xanthine oxidase and neutrophilic NADPH oxidase are commonly invoked to explain reperfusion-induced production of oxygen radicals. The strengths and weaknesses of evidence used to suggest the involvement of both sources are discussed. Evidence is also presented which suggests that xanthine oxidase and neutrophils are redundant yet interactive mechanisms that play an important role in reperfusion injury.
Inauen
W
W
Department of Physiology and Biophysics, Louisiana State University, Shreveport 71130.
Suzuki
M
M
Granger
D N
DN
D000818:Animals; D004730:Endothelium, Vascular / Q000378:metabolism; D005609:Free Radicals; D006801:Humans; D008954:Models, Biological; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D019255:NADPH Oxidases; D009504:Neutrophils / Q000378:metabolism; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D014969:Xanthine Oxidase / Q000378:metabolism
D005609:Free Radicals; D014969:Xanthine Oxidase; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases; D010100:Oxygen