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Exposure of explants of fetal rat lung to dexamethasone, thyroxine, or the methylxanthines, aminophylline and caffeine, resulted in a significant increase in the rate of choline incorporation into all the choline-containing phospholipids. Dexamethasone, aminophylline, or caffeine treatment also resulted in an increase in the percentage of radioactivity from [3H]acetate in the surfactant-associated phospholipids, disaturated phosphatidylcholine, and phosphatidylglycerol and a corresponding decrease in the membrane phospholipids. Exposure to thyroxine had different effects. Only aminophylline and caffeine produced an increase in the rate of incorporation of acetate into phospholipid. Differences were also observed in the activities of enzymes of phospholipid synthesis. The activity of cholinephosphate cytidylyltransferase was increased by dexamethasone and that of choline kinase and lysolecithin acyltransferase by aminophylline. Thyroxine had no effect on any of the enzymes examined. All these agents produced a significant decrease in lung glycogen content and a small decrease in the protein-to-DNA ratio. These data indicate that corticosteroids, thyroxine, and the methylxanthines act directly on the fetal lung, but produce different effects and presumably act via different mechanisms.

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We measured the rate of choline incorporation into phosphatidylcholine in lung slices; the glucogen content of the lung; and the activities of pulmonary cholinephosphate cytidylyltransferase, cholinephosphotransferase and phosphatidate phosphatase in the mouse during late fetal and early postnatal development. We also examined the effect of maternal dexamethasone administration on these parameters of fetal lung maturation. There was a development increase in the rate of choline incorporation between 17 days gestation (term is 19 days) and the immediate newborn period. There was also a developmental decrease in the glycogen content of the lung but this did not occur until 18 days. There was a developmental increase in the activities of cholinephosphate cytidylytransferase and phosphatidate phosphatase but little change in the activity of cholinephosphotransferase. Dexamethasone doubled the rate of choline incorporation into phosphatidylcholine at 17 and 18 days gestation. It decreased the glycogen content of the fetal lung by 74% at 18 and 19 days, but had no effect at 16 and 17 days. Dexamethasone increased the activity of pulmonary cholinephosphate cytidylyltransferase by 37% and that of cholinephosphotransferase by 27% at 17 days. It increased the activity of phosphatidate phosphatase by 25% at 16 days and by 32% at 19 days. These data show that the normal development profile of these parameters of fetal lung maturation in the mouse, as well as the effects of glucocorticoids thereon, are generally similar to those in the rabbit and rat. However, stimulation of cholinephosphotransferase by glucocorticoids has not been generally observed in other species. Furthermore, since the changes in the rate of choline incorporation precede those in glycogen depletion, the data suggest that the relationship between phospholipid synthesis and glycogen degradation is not simply that of precursor to product.

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