Enzymes of Lipid Metabolism pp 327-339 | Cite as
The Biosynthesis and Hormonal Regulation of Surfactant Formation
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Abstract
The respiratory distress syndrome (RDS) of the newborn, due to hyaline membrane disease, is caused by an inability of the fetal or neonatal lung to synthesize adequate quantities of the lipoprotein, surfactant (1). It has been demonstrated that the Type II ce1I of the lung synthesizes surfactant, a substance which markedly lowers the surface tension of the lung, preventing alveolar collapse (2). The surface-active properties of surfactant are principally attributable to its phospholipids, the composition of which has several unique features. First, approximately 70–80% of the total glycerophospholipids of surfactant are phosphatidylcholines. Moreover, approximately 50% of the phosphatidylcholines consist specifically of dipalmitoylphosphatidylcholine (DP-PC). Indeed, the principal surface-active properties of surfactant can be accounted for by the action of DP-PC and, to a lesser degree, phosphatidylglycerol (PG). It is the increase in DP-PC that leads to the increase in the lecithin to sphingomyelin (LIS) ratio in amniotic fluid that heralds fetal lung maturation (for recent reviews see ref. 3–5). Recently, Gluck and associates (6) have also suggested that an increase in PG in amniotic fluid, with an associated decrease in phosphatidylinositol, may be considered an additional marker of fetal lung maturation. The lipid composition of surfactant is illustrated in Figure 1.
Keywords
Amniotic Fluid Phosphatidic Acid Phosphatidic Acid Fetal Lung Lamellar BodyReferences
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