Effect of propranolol and cycloheximide on the ethanol-induced increase in liver tryptophan oxygenase activity in starved rats.
Increased supply of tryptophan to the liver, resulting from the lipolytic action of ethanol, is suggested to be responsible for the increased activity of liver tryptophan oxygenase after ingestion of a single large dose of ethanol. This hypothesis was tested using an antilipolytic drug, propranolol, prior to ethanol treatment. It was found that, while propranolol did inhibit the ethanol-induced increase in blood unesterified fatty acids and free tryptophan concentrations, it did not prevent the activation of tryptophan oxygenase by ethanol. In another experiment, where cycloheximide was used to block protein synthesis, it was found that increased protein synthesis rather than decreased protein degradation is probably responsible for the accumulation of liver tryptophan oxygenase after ethanol ingestion.
D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D003513:Cycloheximide / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D008099:Liver / Q000201:enzymology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D014364:Tryptophan / Q000097:blood; D014366:Tryptophan Oxygenase / Q000096:biosynthesis*
D005230:Fatty Acids, Nonesterified; D000431:Ethanol; D014364:Tryptophan; D003513:Cycloheximide; D011433:Propranolol; D014366:Tryptophan Oxygenase; D003345:Corticosterone