Ammonia detoxification by accelerated oxidation of branched chain amino acids in brains of acute hepatic failure rats.
BCAA aminotransferase and BCKA dehydrogenase activities are increased in the mitochondrial fractions from the brains of hepatic failure rats treated with two-thirds removal of CCl4-injured liver. Cerebral leucine decarboxylation was accelerated, and it well correlated with arterial blood ammonia levels. Elevation of brain ammonia content following an intraperitoneal injection of ammonium acetate to hepatic failure rats could be prevented by intravenous infusion of BCAA. Significantly increased brain glutamic acid, glutamine, and alanine contents were noted. These results suggested that accelerated brain BCAA catabolism in acute hepatic failure rats reduce the neurotoxicity of ammonia by promoting the synthesis of glutamic acid and glutamine from BCAA.
D000208:Acute Disease; D000596:Amino Acids / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002208:Caproates / Q000378:metabolism*; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism; D006498:Hepatectomy; D007651:Keto Acids / Q000378:metabolism*; D007930:Leucine / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008107:Liver Diseases / Q000378:metabolism*; D008297:Male; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains
D000596:Amino Acids; D002208:Caproates; D007651:Keto Acids; D000641:Ammonia; C013082:alpha-ketoisocaproic acid; D007930:Leucine