Abstract
A precocious development of UDP-glucuronosyltransferase activity (EC 2.4.1.17) towards o-aminophenol is demonstrated in 15-17 day fetal rat liver in utero after dexamethasone administration to the mother. This stimulation of liver transferase activity in utero is directly proportional to the dose of dexamethasone injected. Precocious development of transferase activity in utero can be affected with the natural glucocorticoid cortisol by multiple injections of large amounts of this hormone into the mother. Transferase activity towards o-aminophenolin fetal lung, kidney and upper alimentary tract can be precociously stimulated by dexamethasone in 17 day fetuses in utero. Natural development of hepatic transferase activity between days 18-20 of gestation is retarded after fetal hypophysectomy by decapitation in utero. Overall glucuronidation of o-aminophenol, as observed in fetal rat liver, is precociously stimulated by dexamethasone. Glucocorticoids, which are known to increase in rat fetuses between days 17-20 of gestation, trigger normal development in utero of hepatic transferase activity towards o-aminophenol which occurs at that time. These hormones are responsible for rise in activity of the enzyme in fetal lung, kidney and upper alimentary tract which occurs during the same gestational period.

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