Source of increased serum aspartate and alanine aminotransferase: cycloheximide effect on carbon tetrachloride hepatotoxicity.
Repeated doses of the protein synthesis inhibitor cycloheximide prevented the increases in rat liver mitochondrial and cytosolic aspartate aminotransferase, in alanine aminotransferase and in protein content observed 24 h after a single carbon tetrachloride injection. Serum aminotransferase activity increases induced by carbon tetrachloride were also decreased as much as 75.7% with cycloheximide. Increased synthesis is, therefore, suggested as an important and sometimes major source of increased serum aminotransferases in hepatocellular injury. This effect of cycloheximide lends support to the hypothesis that the liver enzyme increases after CCl4 are probably due to increased synthesis, in addition to the classically held mechanisms of leakage from necrotic or damaged hepatocytes. This explanation of the mechanisms of release of aminotransferases in rat liver injury would clarify many clinical observations if the same phenomenon were to occur in humans in response to hepatic injury. These data suggest that increased serum aminotransferase activities represent a healing, in addition to a degenerative, process.
D000410:Alanine Transaminase / Q000096:biosynthesis / Q000097:blood*; D000818:Animals; D001219:Aspartate Aminotransferases / Q000096:biosynthesis / Q000097:blood*; D002252:Carbon Tetrachloride Poisoning / Q000201:enzymology*; D056486:Chemical and Drug Induced Liver Injury / Q000201:enzymology*; D003513:Cycloheximide / Q000494:pharmacology*; D003600:Cytosol / Q000201:enzymology; D008099:Liver / Q000201:enzymology; D008297:Male; D008930:Mitochondria, Liver / Q000201:enzymology; D051381:Rats; D011919:Rats, Inbred Strains
D003513:Cycloheximide; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase