Oxygen free radicals and lungs.

Some of the metabolites resulting from the monovalent reduction of O2, superoxide anion and hydroxyl radical, are O2, radicals, whereas H2O2, which is not a radical since having no unpaired electron, is also an active O2 intermediate. These O2 metabolites are formed intracellularly as a result of normal metabolism. Their production can increase following exposure to high O2 concentration, radiations or certain drugs. An increased amount of extracellular O2 metabolites occurs after activation of certain inflammatory cells or during the course of the hypoxanthine-xanthine oxidase reaction. To counteract this oxidative stress, antioxidant defenses exist, whether enzymatic (superoxide dismutase, glutathione peroxidase, catalase, etc.) or nonenzymatic (GSH, vitamin E and C, etc.). Oxidative injury can result from an imbalance between oxidative stress and the defense mechanisms. The main targets are protein, DNA and lipids. The cellular response of the lung is stereotyped and involves cell injury (especially endothelial cells and type I pneumocytes), inflammatory reaction and repair processes.