Ammonia and DNA Metabolism in Hepatic Encephalopathy = Ammonia and DNA Metabolism in Hepatic Encephalopathy

다국어 초록 (Multilingual Abstract)

Significant increases in the activities of hepatic glutamine synthetase and alkaline DNase were observed in rats treated with ammonium chloride for a long period of time. Neither glutamine synthetase nor alkaline DNase activity in the brain was increased prolonged administration of ammonium chloride. These results indicate that, in prolonged treatment with ammonium chloride, the liver has an enough capacity to handle administered ammonia through the formation of urea and glutamine. In rats treated with carbon tetrachloride and ammonium chloride, decrease in hepatic glutamiue synthetase activity and increase in blood ammonia level were observed without any significant change in the activity of brain glutamine synthetase. On the other hand, further decrease in the hepatic glutamine synthetase activity and greater increase in blood ammonia level were found in rats treated with phenobarbital, carbon tetrachloride and ammonium chloride with a significant increase in the activity of brain glutamine synthetase. These observations suggest that when the liver is severely damaged, the brain actively participates in the fixation of free ammonia by increasing the activity of glutamine synthetase.