Platelet-activating factor (PAF)-acetylhydrolase and PAF-like compounds inthe lung: effects of hyperoxia

Platelet-activating factor (PAF)-acetylhydrolase is the enzyme modulating i n tissues and biological fluids the concentration of the proinflammatory fa ctors PAF and PAF-like oxidation products of phospholipids (PAF-like compou nds). We investigated whether there is a relation between PAF-acetylhydrola se activity and the concentration of PAF-like compounds in bronchoalveolar lavage (BAL). We found that alveolar type II cells are an additional source of PAF-acetylhydrolase in BAL beside macrophages. Secretion of PAF-acetylh ydrolase was stimulated by phorbol eater in alveolar type II cells but not in macrophages. Studies in BAL suggested that secreted PAF-acetylhydrolase was bound to alveolar surfactant. Exposure of rats to high oxygen concentra tion reduced the activity of PAF-acetylhydrolase in BAL and macrophages, bu t not in plasma or alveolar type II cells. In contrast, hyperoxia increased the concentration of PAF-like-compounds, lipid hydroperoxides and malonedi aldehyde in plasma but not in BAL. Therefore, we conclude that neither the oxidant-induced decrease of the PAF-acetylhydrolase activity nor the direct peroxidation of surfactant lipids in the alveoli provide a likely mechanis m for hyperoxia-induced lung injury. Instead, lung injury is apparently cau sed by lipid peroxidation in plasma rather than by high oxygen pressure in the alveoli. (C) 2001 Elsevier Science B.V. All rights reserved.