Cerebral Ammonia Metabolism in Hyperammonemic Rats
Article first published online: 5 OCT 2006
Journal of Neurochemistry
Volume 44, Issue 6, pages 1716–1723, June 1985
How to Cite
Cooper, å. J. L., Mora, S. N., Cruz, N. F. and Gelbard, A. S. (1985), Cerebral Ammonia Metabolism in Hyperammonemic Rats. Journal of Neurochemistry, 44: 1716–1723. doi: 10.1111/j.1471-4159.1985.tb07159.x
- Issue published online: 5 OCT 2006
- Article first published online: 5 OCT 2006
- Received July 18, 1984; accepted November 20, 1984.
- Cerebral ammonia metabolism;
- Portacaval-shunted rats;
- Glutamine synthetase;
The short-term metabolic fate of blood-borne [13N]ammonia was determined in the brains of chronically (8- or 14-week portacaval-shunted rats) or acutely (urease-treated) hyperammonemic rats. Using a “freezeblowing” 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 (amide). However, 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-week 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 present findings are discussed in the context of the known deleterious effects on the CNS of high ammonia levels in a variety of diseases.