Role of thyroid hormones in the normal and glucocorticosteroid hormone-induced evolution of carbamoylphosphate synthase (ammonia) and arginase activity in perinatal rat liver.

Administration of thyroid hormones causes a dose-dependent increase in carbamoylphosphate synthase (ammonia) and arginase activities in fetal rat liver but not in neonatal rat liver. Simultaneous administration of thyroid and glucocorticosteroid hormones enhances enzyme accumulation still further in the fetus. When administered before birth, the relative potencies of T4 and reverse T3, compared to T3 are 20--25% and 1--20%, respectively. Both before and after birth, thyroid hormones enhance DNA content of the liver. Hypophysectomy of rat fetus reduces the carbamoylphosphate synthase activity level in hepatocytes to 30--40% of that in intact animals. Thyroid and glucocorticosteroid hormone administered individually to hypophysectomized animals stimulate enzyme activity 2- to 3-fold; and if administered simultaneously, 4- to 6-fold. Premature delivery with continuation of thyroid and/or glucocorticosteroid hormone treatment started before birth shows uninterrupted enzyme accumulation profiles. Delaying birth by progesterone treatment of the dam leads to uninterrupted but reduced rates of enzyme accumulation in hepatocytes.