Subcutaneous administration of hydrocortisone acetate to the newborn rat produces a premature induction of hepatic tryptophan oxygenase consisting of a transient rise in activity 6-8 h after treatment, followed by a second sustained rise beginning 40 h later, which plateaus at 10 days of age. Cycloheximide treatment at the midpoint of this second elevation inhibits protein synthesis, but not tryptophan oxygenase activity. In older animals, cycloheximide treatment does both. Tryptophan administration at this midpoint rapidly elevates tryptophan oxygenase activity. This elevation can be partially blocked by treatment with actinomycin D within 1 h of tryptophan administration, but not thereafter. Actinomycin treatment is ineffective in blocking the tryptophan-induced rise in older animals. Administration of hydrocortisone acetate to 5- and 10-day-old pups leads to a more rapid and sustained rise in tryptophan oxygenase activity without appearance of a transient induction phase. Neither tryptophan alone, δ-aminolevulinic acid alone, nor tryptophan plus δ-aminolevulinic acid prematurely induces tryptophan oxygenase in newborn or 5-day-old rats.