Abstract
Activated species of oxygen have been implicated as mediators of some acute lung injury. In adult respiratory distress syndrome (ARDS), polymorphonuclear leukocytes accumulate in the lung and release excessive amounts of O2-derived products into the extracellular environment. The effects of these O2 products on lung tissue are multiple. In particular, they can initiate lipid peroxydation in cellular membranes. Excessive lipid peroxydation in membranes destroys cells such as vascular endothelium. Lipid peroxides are also detrimental to cellular functions. Lipid peroxydation could then play a role in the pathogenesis of ARDS.
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