Mørland J, Stowell L, Gjerde H
Alcohol. 1985 Mar-Apr;2(2):255-9. doi: 10.1016/0741-8329(85)90055-2.
Acute administration of ethanol (4.0 g/kg) intragastrically or intraperitoneally induced rat liver tryptophan oxygenase (TO) activity 3-4 fold 4-5 hr later. Ethanol administration increased the concentration of plasma free tryptophan and free fatty acids. Pretreatment with a beta-receptor blocker, propranolol, modified the latter responses without affecting the TO induction due to ethanol. The rise of the level of plasma free tryptophan due to ethanol was too small to influence TO activity. Liver tryptophan concentration and TO half-life was unchanged after ethanol administration. Ethanol administration increased the concentration of plasma corticosterone sufficiently to increase TO activity. Pretreatment with a glucocorticoid antagonist blocked this TO response to ethanol. The increased TO activities found after ethanol or corticosterone treatment were influenced in the same manner and to the same extent by cycloheximide. Taken together it is concluded that ethanol induces TO through a rise of glucocorticoid hormones and not by a tryptophan-linked mechanism.
