Acute ethanol effects on rat liver tryptophan oxygenase and tyrosine aminotransferase.
In starved rats, ethanol administered acutely enhances tryptophan oxygenase (TO) and tyrosine aminotransferase (TAT) activities. Ethanol also inhibits the early phase of the cortisol-mediated TO and TAT induction. Ethanol administered at the same time as tryptophan does not modify the tryptophan-mediated TO and TAT induction. In cortisol-pretreated rats, ethanol enhances the subsequent TO and TAT induction whereas no additive effects are observed when ethanol is injected together with tryptophan. These results suggest that ethanol mimics the effects of tryptophan on TO and TAT activities. In fed animals, ethanol alone does not result in increased TO and TAT activities, but inhibits their cortisol induction. It increases TO activities when given together with a tryptophan dose which, when given alone, does not enhance these activities. It is suggested that the observed inhibitory effects of ethanol on cortisol-mediated TO and TAT induction in starved and fed animals are related to a defective cortisol transport in the liver cells.
D000435:Alcoholic Intoxication / Q000201:enzymology*; D000818:Animals; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D006854:Hydrocortisone / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014364:Tryptophan / Q000494:pharmacology; D014366:Tryptophan Oxygenase / Q000378:metabolism*; D014444:Tyrosine Transaminase / Q000378:metabolism*
D000431:Ethanol; D014364:Tryptophan; D014366:Tryptophan Oxygenase; D014444:Tyrosine Transaminase; D006854:Hydrocortisone