CEREBRAL AMMONIA METABOLISM IN HYPERAMMONEMIC RATS
CEREBRAL AMMONIA METABOLISM IN HYPERAMMONEMIC RATS
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DOI:
10.1111/j.1471-4159.1985.tb07159.x
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发表时间:
1985-01-01
影响因子:
4.7
通讯作者:
GELBARD, AS
中科院分区:
文献类型:
--
作者:
COOPER, AJL;MORA, SN;GELBARD, AS
The short-term metabolic fate of blood-borne [13N]ammonia was determined in the brains of chronically (8- or 14-wk portacaval-shunted rats) or acutely (urease-treated) hyperammonemic rats. Using a freeze-blowing technique it was shown that the overwhelming route for metabolism of blood-borne [13N]ammonia in normal, chronically hyperammonemic and acutely hyperammonemic rat brain was incorporation into glutamine (amine). The rate of turnover of [13N]ammonia to L-[amide-13N]glutamine was slower in the hyperammonemic rat brain than in the normal rat brain. The activities of several enzymes involved in cerebral ammonia and glutamate metabolism were also measured in the brains of 14-wk portacaval-shunted rats. The rat brain appears to have little capacity to adapt to chronic hyperammonemia because there were no differences in activity compared with those of weight-matched controls for the following brain enzymes involved in glutamate/ammonia metabolism: glutamine synthetase, glutamate dehydrogenase, aspartate aminotransferase, glutamine transaminase, glutaminase and glutamate decarboxylase. The findings are discussed in the context of the known deleterious effects on the CNS of high ammonia levels in a variety of diseases.