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hyperammonemia/l tyrosin
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Tyrosine uptake and regional brain monoamine metabolites in a rat model resembling congenital hyperammonemia.
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Hyperammonemia found in congenital disorders has a toxic effect on the central nervous system. Disturbances of brain neurotransmitter metabolism have been proposed, such as an increased transport of tryptophan into the brain and an increased flux through the serotonin pathway. Results concerning the
Protein tyrosine nitration in hyperammonemia and hepatic encephalopathy.
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Hepatic encephalopathy is seen as a clinical manifestation of a chronic low grade cerebral edema, which is thought to trigger disturbances of astrocyte function, glioneuronal communication, and finally HE symptoms. In cultured astrocytes, hypoosmotic swelling triggers a rapid oxidative stress
[Clinicopathological study of multiple myeloma associated with hyperammonemia].
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Of 5 multiple myeloma patients with hyperammonemia, autopsy was performed in 4 patients, while amino acid metabolism was examined in 3 patients. As a result they were classified into the following 3 types; A, liver dysfunction and severe liver infiltration of myeloma cells. B, severe liver
Hyperammonemia and anorexia in Morris hepatoma-bearing rats.
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Inoculation of Buffalo rats with Morris hepatoma produced significant anorexia within four weeks and reduced body weight within two weeks. Blood ammonia concentration was increased by 113% when the rats were euthanized, five days after the development of anorexia. Infusing ammonium salts into normal
Lipopolysaccharide-induced tyrosine nitration and inactivation of hepatic glutamine synthetase in the rat.
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Glutamine synthetase (GS) in the liver is restricted to a small perivenous hepatocyte population and plays an important role in the scavenging of ammonia that has escaped the periportal urea-synthesizing compartment. We examined the effect of a single intraperitoneal injection of lipopolysaccharide
Urea cycle disorders, hyperammonemia and neurotransmitter changes.
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In congenital urea cycle disorders, detoxification of ammonia is impaired, leading to hyperammonemia. Ammonia is the major component causing the acute neurological disturbances. It may influence the supply of substrate and its transport at the blood-brain barrier (BBB) which results in alterations
A novel mutation in GLUD1 causing hyperinsulinism-hyperammonemia in a patient with high density of homozygosity on microarray: a case report.
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BACKGROUND
Hyperinsulinism-hyperammonemia syndrome is the second most common cause of congenital hyperinsulinism and is easily treated with diazoxide; however, the symptoms in our patient were very difficult to control with typical medical therapy. To the best of our knowledge, neither our patient's
Aminograms during continuous hemodiafiltration in the treatment of hyperammonemia due to ornithine transcarbamylase deficiency.
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BACKGROUND
Hyperammonemia caused by ornithine transcarbamylase (OTC) deficiency can be properly managed by continuous arteriovenous hemodiafiltration (CAVHDF). Removal of amino acids (AA) during CAVHDF has not been thoroughly investigated. AA losses in patients with urea cycle defects due to
Brain phenylalanine and tyrosine levels and hepatic encephalopathy induced by CCl4 in rats.
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The correlation between the levels of brain aromatic amino acids and hepatic encephalopathy induced by CCl4 was investigated in rats. CCl4 (1.0 ml/kg three times per week for over 10 weeks) caused hyperammonemia and hepatic encephalopathy in rats. The brain levels of aromatic amino acids, especially
Exploratory investigation on nitro- and phospho-proteome cerebellum changes in hyperammonemia and hepatic encephalopathy rat models.
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Hepatic encephalopathy (HE) is a neurological disease associated with hepatic dysfunction. Current knowledge suggests that hyperammonemia, related to liver failure, is a main factor contributing to the cerebral alterations in HE and that hyperammonemia might impair signal transduction associated
Hyperammonemia, increased brain neutral and aromatic amino acid levels, and encephalopathy induced by cyanide in mice.
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The correlation among hyperammonemia, brain neutral amino acid, and encephalopathy induced by cyanide was investigated in mice. Subcutaneous injection of 10 mg/kg of potassium cyanide increased the levels of blood ammonia by 2.5-fold as compared to those of the corresponding controls and caused loss
Intra- and extracellular amino acid concentrations in portacaval-shunted rabbits. Role of hyperammonemia and effects of branched-chain amino acid-enriched parenteral nutrition.
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Intra- and extracellular amino acid concentrations were measured in rabbits in order to elucidate the possible role of hyperammonemia in lowering the postabsorptive plasma levels of branched-chain amino acids (BCAA) and to assess the effects of BCAA-enriched total parenteral nutrition (TPN) on the
Ornithine loading did not prevent induced hyperammonemia in a patient with hyperornithinemia-hyperammonemia-homocitrullinuria syndrome.
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Impairment of urea cycle function in hyperornithinemia-hyperammonemia-homocitrullinuria syndrome is presumably caused, in some patients, by deficient transport of ornithine from cytoplasm into mitochondria. We studied the effect of L-ornithine on L-alanine-induced hyperammonemia in a French-Canadian
Serum amino acid disturbance in multiple myeloma with hyperammonemia.
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From October 1987 to November 1993 we evaluated the serum levels of ammonia and amino acids in 85 patients with multiple myeloma. Six of the 85 cases of multiple myeloma demonstrated hyperammonemia and none of the known causes of hyperammonemia, such as liver failure, could be identified in these
RNA oxidation and zinc in hepatic encephalopathy and hyperammonemia.
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Hepatic encephalopathy is a neuropsychiatric manifestation of acute and chronic liver failure. Ammonia plays a key role in the pathogenesis of hepatic encephalopathy by inducing astrocyte swelling and/or sensitizing astrocytes to swelling by a heterogeneous panel of precipitating factors and
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