Lung Phosphatidylcholine Synthesis and Cholinephosphotransferase Activity in Anencephalic Rat Fetuses with Corticosteroid Deficiency

Abstract

Summary: Adrenocortical insufficiency was produced in rat fetuses by surgical decapitation. These animals show low plasma corticosterone levels compared to littermate controls. Lung slices from anencephalic fetuses were found to have reduced incorporation of [¹⁴C]choline into phosphatidylcholine, hence diminished choline pathway activity; this abnormality was present at 21 days of gestation but not at term. Cholinephosphotransferase (CPT), the terminal catalyst of the choline pathway, also showed diminished activity in lungs of anencephalic fetuses, with a mean of 120 pmol/min/mg protein compared to a control value of 190. Dexamethasone treatment of these animals for 6–12 hr led to enhanced choline incorporation rates. Corticosteroid administration also restored CPT activity and even elevated the enzyme to a mean level (340 pmol/min/mg protein) greater than that found in normal fetuses at 21–22 days of gestation. The early pulmonary biochemical effects of dexamethasone in this model were not accompanied by recognizable ultrastructural changes. Speculation: It is proposed that glucocorticoids act to influence the timing of lung biochemical development relative to phosphatidylcholine synthesis. Increased amounts of the hormone appear to be sufficient but not necessary for this effect since augmented choline pathway rates eventually occur in the absence of the corticosteroid stimulus.