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PubMed1988

Hyperammonemia in anorectic tumor-bearing rats.

Plasma ammonia concentrations were significantly elevated by 150% in anorectic rats bearing methylcholanthrene sarcomas. Assessment of ammonia levels in blood draining these sarcomas indicated nearly a 20-fold increase as compared with venous blood in control rats, suggesting the tumor mass as the source of this increase in ammonia. Infusing increasing concentrations of ammonium salts produced anorexia and alterations in brain amino acids in normal rats that were similar to those observed in anorectic tumor-bearing rats. Therefore, these results suggest that ammonia released by tumor tissue may be an important factor in the etiology of cancer anorexia.

Amino Acids↗
PubMed1985

Differential response of enzymes of glutamate metabolism in neuronal perikarya and synaptosomes in acute hyperammonemia in rat.

Activity levels of the enzymes of glutamate metabolism were determined in the neuronal perikarya and synaptosomes isolated from the cerebral cortex of normal and hyperammonemic rats. In neuronal perikarya, the activities of glutamate dehydrogenase, aspartate, alanine aminotransferases and glutamine synthetase were elevated in hyperammonemic states. In synaptosomes, glutamate dehydrogenase and aspartate aminotransferase were suppressed, while glutamine synthetase and glutaminase were elevated. These results suggested the involvement of neuronal perikarya in ammonia detoxification at least in acute hyperammonemic states.

Alanine Transaminase↗
PubMed1991

Cloning and sequence of a cDNA encoding human carbamyl phosphate synthetase I: molecular analysis of hyperammonemia.

Carbamyl phosphate synthetase I (CPSI) is the first enzyme involved in urea synthesis. CPSI deficiency is an autosomal recessive disorder characterized by hyperammonemic coma in the neonatal period. To analyze the enzyme and gene structures, and to elucidate the nature of mutations in CPSI deficiency, we isolated cDNA clones encoding human liver CPSI. Oligo(dT)-primed and random primer human liver cDNA libraries in lambda gt11 were screened using 5', middle, and 3' fragments of the rat CPSI cDNA as probes. Seven positive clones covered the full-length cDNA sequence with an open reading frame encoding a precursor polypeptide of 1500 amino acids (aa) (deduced Mr, 164,828) with a putative N-terminal presequence of 38 or 39 aa, a 5'-untranslated sequence of 118 bp and a 3'-untranslated sequence of 597 bp. Comparison with the rat CPSI cDNA showed that the deduced aa sequence of the human liver CPSI precursor is 94.4% identical to the rat enzyme precursor. A molecular analysis was made of the genomic DNA from three patients with CPSI deficiency. Heterogeneity of hybridized fragments that may or may not be the cause of the deficiency was apparent on the DNA blots from tissues from one patient.

Amino Acid Metabolism, Inborn Errors↗
PubMed1998

Region-specific changes in CNS muscarinic acetylcholine receptors in a rat model of hyperammonemia.

Multiple neurotransmitter systems have been implicated in the etiology of cerebral dysfunction in acute and chronic hyperammonemic states. Involvement of the neurotransmitter systems of glutamate and gamma-aminobutyric acid has been reported, whereas not much information is available on the role of the cholinergic system in the etiology of hyperammonemic states. In the present investigation, muscarinic acetylcholine receptors (mAChR) were studied, using tritium-labelled quinuclidinyl benzilate ([3H]QNB), in rats administered ammonium acetate (AA), and the changes in the treated rats were compared with measurements in normal rats. The presence of two affinity (high and low) systems for [3H]QNB binding was observed in the cerebral cortex (CC), while a single affinity system was seen in the cerebellum (CE) and pons-medulla (PM). A decrease in the Bmax of both the high and low affinity systems for [3H]QNB binding was observed in the CC with no significant change in the Kd values in rats administered an acute dose of AA (25 mmol/kg of body weight). The Bmax values were unaltered in CE and PM, but a significant increase in the Kd value was observed in the CE. Studies of [3H]QNB binding in the presence of pirenzepine (a specific antagonist of M1 receptors) indicated the predominance of non-M1-type (M2, M3, M4, and M5) receptors (85-90% of the total specific binding) in the CE and PM, whereas in the CC, 60% was represented by non-M1 and 40% by M1 receptors. Reduction in [3H]QNB binding to M1 receptors was observed in the CC and PM of rats administered an acute dose of AA. Administration of lower doses of AA (2.5 mmol/kg of body weight) had no effect on CC and CE mAChRs, while an increase in non-M1 and a decrease in M1 receptors was observed in the PM. As the neurotransmitter receptors play a key role in signal transduction, the observed changes in receptor functions may be responsible for some of the behavioral changes reported in hyperammonemic states.

Ammonia↗