INFLUENCE OF HORMONES ON THE BIOCHEMICAL DEVELOPMENT OF FETAL-RAT LUNG IN ORGAN-CULTURE .1. ESTROGEN

It was recently demonstrated that 17β-estradiol enhances phosphatidylcholine synthesis in fetal lung in vivo. In order to determine whether estrogen acts directly on the lung, we examined the influence of 17β-estradiol on phospholipid and glycogen metabolism in explants of 18 day fetal rat lung in organ culture. Exposure of the explants to 17β-estradiol resulted in significant stimulation of [Me-3H]choline incorporation into phosphatidylcholine, disaturated phosphatidylcholine and sphingomyelin. Incorporation of [3H]acetate into total phospholipid was increased by 63% (P < 0.001). Incorporation into individual phospholipids was similarly increased, except for that into phosphatidyl-glycerol which was enhanced by 111% (P < 0.005). When the data were expressed as the percentage of radioactivity from [3H] acetate in the various phospholipid fractions, it was found that there was a 29% increase in the phos-phatidylglycerol fraction (P < 0.005) and a 12% reduction in phosphatidyl-inositol plus phosphatidylserine combined (P < 0.005). There was no significant change in the percentage of radioactivity in any of the other phospholipid fractions, or in the activity of any of the enzymes of phospholipid synthesis examined. Estrogen treatment also resulted in a decrease in the glycogen content (P < 0.05), but no change in the protein/DNA ratio. These data indicate that estrogen acts directly on the fetal lung and stimulates the incorporation of choline and acetate into phospholipids. It may specifically enhance incorporation into phosphatidylglycerol, the second most abundant phospholipid in pulmonary surfactant. © 1979.