Abstract
Two major pathways for the biosynthesis of the major surface-active lipid of lung, dipalmitoyl lecithin, have been described and the relative activities of each pathway in mammalian lung compared. In normal adult lung the cytidine disphosphocholine (CDP-choline) pathway is quantitatively most important for total lecithin synthesis. Synthesis of saturated lecithin is depressed by interruption of pulmonary blood flow and atelectasis and by hypoxia. Synthesis of lecithin by N-methyltransferase is relatively less important in normal adult lung and is depressed by high concentrations of oxygen. Methyltransferase activity is less depressed by pulmonary artery ligation and is increased by hypoxia and in the late stages of fetal life. Purified N-methyltransferase isolated from lung selectively forms saturated lecithin, is rapidly inactivated on exposure to oxygen, is protected by sulfhydryl agents and is associated with lamellated particles containing significant amounts of lipid.