Treatment of Wistar rats with a single dose of hydrocortisone acetate resulted in a transient induction of tyrosine aminotransferase (TAT) in the liver. TAT activity and the level of TAT mRNA increased 4-6 h after addition of hydrocortisone acetate (induction phase) and declined thereafter (deinduction phase). TAT activity and TAT mRNA failed to respond to readdition of fresh hydrocortisone acetate during the deinduction period, but cycloheximide treatment at this period increased the level of TAT mRNA. Hydrocortisone acetate alone and cycloheximide alone or after hydrocortisone acetate treatment stimulated the rate of TAT gene transcription. TAT displayed a low activity in the rat heart, brain and kidney, and was not induced by hydrocortisone acetate in these tissues. In addition to liver, TAT mRNA was found in heart, brain and kidney, but in the latter three tissues its amount was about one tenth only as in the liver, which was consistent with different levels of TAT activity. Upon hydrocortisone acetate treatment the TAT mRNA levels in brain and heart remained unchanged.