Abstract
Increasing use of oxygen in clinical practice has provided new impetus for determining mechanisms of acute pulmonary oxygen toxicity. The pathophysiology of lungs exposed to oxygen in vivo and in vitro suggests a direct toxic effect of hyperoxia upon lung cells, with variation in sensitivity to injury among cell types. The currently accepted primary mechanism for oxygen-induced cellular injury is enhanced oxygen-derived free radical generation with subsequent oxidative attack upon basic cell constituents. The major intracellular sources of increased free radicals are undetermined, but there is sufficient evidence that the extracellular contribution, specifically from PMN leukocyte influx into lungs is not critical to lethal pulmonary oxygen toxicity. Cellular protection is provided by intracellular enzymatic and nonenzymatic anti-oxidant defenses, which can be manipulated by experimental treatments to alter survival in O2. Our increasing knowledge of the mechanisms of oxidant toxicity may lead to improved strategies for early detection of lung damage and for the prevention or treatment of injury.
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