Dihydrotestosterone inhibits fibroblast-pneumonocyte factor-mediated synthesis of saturated phosphatidylcholine by fetal rat lung cells.

Abstract

Dihydrotestosterone has previously been found to inhibit pulmonary surfactant production in vivo. In the present study, we have investigated the effects of this androgen on the fetal lung fibroblast and type II cell in culture. Addition of 1 X 10(-8) M cortisol to organotype cultures stimulates the synthesis of radiolabelled saturated phosphatidylcholine; however, preincubation of such cultures with 1 X 10(-8) M dihydrotestosterone completely blocks cortisol stimulation of saturated phosphatidylcholine synthesis without affecting basal activity. Cortisol treatment of fetal lung fibroblasts stimulates the production of fibroblast-pneumonocyte factor; pre-treatment with dihydrotestosterone blocks this stimulation. Fibroblast-pneumonocyte factor stimulates the synthesis of saturated phosphatidylcholine by type II pneumonocytes; this effect is also blocked by dihydrotestosterone pre-treatment. I conclude that dihydrotestosterone blocks cortisol-inducible saturated phosphatidylcholine synthesis by inhibiting the production and activity of fibroblast-pneumonocyte factor in vitro.