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SummaryThe soluble fraction from adult rat lung type II cells stimulated the transfer of various phospholipids between either fiposomes or rat, lung microsomes and rat lung mitochon~a.Compared to whole lung, type II cells are highly enriched in transfer activity suggesting that phospholipid-tr~sfer proteins play a role in the transport of surfactant phospholipids. Sephadex chromatography of pH 5.1 supematant from type II cells yielded only one fraction catalysing the transfer of phosphatidylcholine, phosphatidylglycerol and phosphatidylethanolamine, while chromatography of pH 5.1 supernatant from whole lung yielded in addition a specific phosphatidylcholinetransfer and a specific phosphatidylgly~erol-transfer protein.Disaturated phosphatidylcholine and phosphatidylglycerol are the major lipid components of pulmonary surfactant which lowers surface tension in the alveoli and prevents lung collapse during expiration [l--3] . Alveolar epithelial type II cells are considered to be the site of surfactant synthesis f 3-51. These cells contain unique subcellular structures, the lamelar bodies, which store the surfact~t prior to its secretion onto the alveolar surface [ 51. The mechanism via which the surfactant lipids are transferred from their site of synthesis in the type II cell to the storage organelle is unknown. Several reports [ 6-101 suggest that phospholipid-transfer proteins are involved in the intracellular transport of surfactant phospholipids. Recently, we demonstrated the presence in whole rat lung of two specific transfer proteins, one catalysing the transfer of phosphatidylcholine and the other that of phosphatidylglycerol. In addition, a third protein or mixture of proteins was isolated from whole rat lung cytosol which catalysed the trans-

Isolated alveolar epithelial type II cells were exposed to paraquat and to hyperoxia by gas diffusion through the thin Teflon bottom of culture dishes. After exposure, type II cells were further incubated in the presence of labelled substrates to assess their capacity to synthesize lipids. Hyperoxia alone (90% O2; 5 h) had minor effects on lipid metabolism in the type II cells. At low paraquat concentrations (5 and 10 microM), hyperoxia enhanced the paraquat-induced decrease of [Me-14C]choline incorporation into phosphatidylcholines. The incorporation rates of [Me-14C]choline, [1-14C]palmitate, [1-14C]glucose and [1,3-3H]glycerol into various phospholipid classes and neutral lipids were decreased by paraquat, depending on the concentration and duration of the exposure. The incorporation of [1-14C]acetate into phosphatidylcholines, phosphatidylglycerols and neutral lipids appeared to be very sensitive to inactivation by paraquat. At 5 microM-paraquat the rate of [1-14C]acetate incorporation was decreased to 50% of the control values. The rate of [1-14C]palmitate incorporation into lipids was much less sensitive; it even increased at low paraquat concentrations. At 10 microM-paraquat both NADPH and ATP were significantly decreased. It is concluded that lipid synthesis in isolated alveolar type II cells is extremely sensitive to paraquat. At low concentrations of this herbicide, lipid synthesis, and particularly fatty acid synthesis, is decreased. The effects on lipid metabolism may be partly related to altered NADPH and ATP concentrations.