Oxygen radicals in complement and neutrophil-mediated acute lung injury.
The development of experimental acute lung injury following systemic complement activation is closely related to availability of blood neutrophils. Although tissue-destructive neutrophil-derived proteinases may play a supportive role in acute pulmonary injury, it appears that oxygen radical constitute the major neutrophil product responsible for acute damage of lung tissues and cells. Intravascular activation of neutrophils by the chemotactic complement peptide C5a is related to the generation of superoxide anion. Dismutation of superoxide to hydrogen peroxide and its iron-mediated conversion to hydroxyl radical appear to constitute in vivo events that ultimately lead to acute lung microvascular injury.
D000818:Animals; D003167:Complement Activation; D003182:Complement C5 / Q000502:physiology; D015936:Complement C5a; D004546:Elapid Venoms; D010450:Endopeptidases / Q000502:physiology; D005609:Free Radicals; D008168:Lung / Q000276:immunology / Q000503:physiopathology; D055370:Lung Injury; D008297:Male; D015260:Neprilysin; D009504:Neutrophils / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism*; D051381:Rats
D003182:Complement C5; D004546:Elapid Venoms; D005609:Free Radicals; C016310:cobra venom factor; D015936:Complement C5a; D010450:Endopeptidases; D015260:Neprilysin; D010100:Oxygen