Corticosteroid metabolism in fetal and newborn mice

Abstract

Corticosterone-4-14C was injected intravenously into pregnant mice and fetal tissues were removed after 30 min. Extracts were chromatographed on paper from which zones were eluted and counted. Most counts occurred in the zones representing corticosterone (cpd. B) and 11-dehydrocorticosterone (cpd. A). At a fetal size up to 5 mm crown–rump length (about 11 days), cpd. A constituted 45% of the total counts; this rose as high as 96% (average 80%) in fetuses up to 15 mm. This appeared to be due to increased dehydrogenase activity in fetal tissue; the placenta was also highly active throughout pregnancy. In contrast, late in gestation cpd. A dropped to 24% and this was attributed to the appearance of reductase activity in fetal liver which reduces the metabolite. In young mice for the first 3 weeks of postnatal life the ratio A/B was about 1. Cortisol-4-14C was converted to cortisone but at a slower rate. It was concluded that the 11β-hydroxysteroid dehydrogenase system plays an important role in protecting the fetus from high maternal levels of corticosteroid, but could in some circumstances result in the continued catabolism of biologically active hormone in neonatal life.