Studies of Rat Liver and Kidney Enzymes

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Abstract
In an effort to characterize enzymatically the biochemical changes in rats during hyperammoniemia and amino acid loading, the responses of rat tissue enzymes following the intragastric administration of ammonium acetate, l-glutamine, l-arginine hydrochloride, dl-alanine and l-monosodium glutamate for extended periods of time have been studied. Liver arginase specific activity decreased with both ammonium acetate and l-glutamine and was not significantly changed by l-arginine hydrochloride administration. Kidney arginase specific activity increased in short-term experiments following both ammonium acetate and l-glutamine administration and was followed by a return toward control values in the longer experiments suggesting an adaptive response of this enzyme. Kidney arginine synthetase specific activity increased after administration of all of the following nitrogenous substances: ammonium acetate, glutamine, arginine, alanine and monosodium glutamate. Liver and kidney glutamic oxaloacetic transaminase and liver arginase specific activities were not increased following the administration of any nitrogenous substance administered and in most cases showed a marked decline. Liver glutamotransferase and glutamic dehydrogenase specific activity increased following ammonium acetate administration in contrast to any significant change after glutamine. Liver glutamic dehydrogenase activity was also increased after l-arginine hydrochloride administration. Kidney glutaminase i specific activity was not significantly altered following either ammonium acetate or any other nitrogenous substance tested. Liver ornithine transcarbamylase and arginine synthetase specific activities were not significantly altered by any of the substances nor were liver histidase specific activities changed after ammonium acetate and liver glutaminase i following ammonium acetate and glutamine administration. The relationship of these enzyme changes to aspects of urea and ammonia metabolism is discussed.