Ethanol was given as short‐term treatment to intact animals in the following ways: Orally in mixture with sucrose as drinking fluid ad libitum for one or 18‐21 hrs, or intraperitoneally (i.p.) as a single dose (2.5 or 3.3 g/kg rat). Ethanol was also added to perfusates (final concentration 0.2 %) of isolated livers. Short‐term ethanol treatment (in vivo) was also given to animals which had been pretreated with ethanol for 3‐4 weeks.I.p. injection of ethanol caused a significant rise in tryptophan oxygenase (TO)‐activity (337 %) and plasma corticosterone (approximately 400 %), while consumption of ethanol only slightly increased the enzyme activity without any significant effects on steroid hormone concentration. The administration of cycloheximide (1.5 mg/kg) abolished the increase in TO‐activity normally found after i.p. injection of ethanol. Ethanol did not affect the basal TO‐activity in the perfused liver, but slightly increased the effect of dexamethasone induction. TO degradation measured after administration of cycloheximide (20 μg/ml) was unchanged by ethanol in the perfused liver. An i.p. injection of ethanol increased the TO‐activity (268 %) in ethanol‐pretreated rats, but to a smaller extent than in normal animals. The TO‐activity measured after consumption in ethanol‐pretreated rats was significantly reduced. It was concluded that the acute stimulatory effect of ethanol on TO‐activity was due to the rise in plasma corticosterone which induced enzyme synthesis. Long‐term consumption of ethanol was accompanied by reduced basal TO synthesis as well as by reduced enzyme induction after acute ethanol treatment.