citrulline/oedeem

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Accumulation of cytotoxins during the development of seizures and edema after hypoxic-ischemic injury in late gestation fetal sheep.

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Several hours after an hypoxic-ischemic injury to the developing brain, hyperemia, then seizures, edema, and infarction can develop. The roles of nitric oxide (NO) synthesis and excitotoxin accumulation during these later phases of injury are not known. The time course of extracellular levels of

Citrulline and ammonia accumulating in citrullinemia reduces antioxidant capacity of rat brain in vitro.

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Citrullinemia is an inborn error of the urea cycle caused by deficient argininosuccinate synthetase, which leads to accumulation of L-citrulline and ammonia in tissues and body fluids. The main symptoms include convulsions, tremor, seizures, coma, and brain edema. The pathophysiology of the

The role of nitric oxide in edema formation in L-arginine-induced acute pancreatitis.

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BACKGROUND Nitric oxide (NO) has been implicated in the regulation of the pancreatic circulation, the promotion of the capillary integrity, and the inhibition of leukocyte adhesion. OBJECTIVE To investigate the rates of changes in the pancreatic constitutive NO synthase (cNOS) and inducible NOS

[Type II citrullinemia triggered by acetaminophen].

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We report a 19-year-old man with type II citrullinemia triggered by the administration of acetaminophen when he caught a cold. He was admitted to our hospital of impairment of consciousness and abnormal behaviors. On admission he was comatose and laboratory data revealed respiratory alkalosis which

L-arginine attenuates trauma-hemorrhage-induced liver injury.

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OBJECTIVE Liver injury is common after trauma-hemorrhage for which the underlying mechanism is not clear. Although administration of the essential amino acid L-arginine has been reported to restore the depressed cardiovascular functions and cell-mediated immune responses after trauma-hemorrhage, it

Perinatal pathology casebook.

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Citrullinemia, a rare inborn error of metabolism, is characterized by a deficiency of argininosuccinic acid synthetase that results in large increases in plasma ammonia, citrulline, and glutamine, with normal acid-base balance. The neurologic symptoms vary from poor feeding, vomiting, and

A profile of amino acid and catecholamine levels during endotoxin-induced acute lung injury in sheep: searching for potential markers of the acute respiratory distress syndrome.

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The identification of plasma markers of the course of the acute respiratory distress syndrome (ARDS) is needed to improve its treatment and to further advance the development of new therapeutic agents. The status of markers of lung injury in ARDS is reviewed and some new potential markers are

Ethanol and age enhances fluoride toxicity through oxidative stress and mitochondrial dysfunctions in rat intestine.

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Fluoride toxicity and alcohol abuse are the two serious public health problems in many parts of the world. The current study was an attempt to investigate the effect of alcohol administration and age on fluoride toxicity in rat intestine. Six and 18 months old female Sprague Dawley rats were exposed

A case of adult-onset type II citrullinemia--deterioration of clinical course after infusion of hyperosmotic and high sugar solutions.

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BACKGROUND Adult-onset type II citrullinemia (CTLN2) is an autosomal recessive disorder caused by mutations of SLC25A13 gene encoding citrin and is characterized by recurrent encephalopathy with hyperammonemia. Factors affecting disease progression remain unknown. We report a case with CTLN2, whose

[Protection of naoyi-an granule in ischemic brain injury secondary to intracerebral hemorrhage in rats].

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OBJECTIVE To explore the protective effect and its mechanism of the traditional Chinese medicine complex, naoyi-an granule(NYAG), on intracerebral hemorrhage(ICH) in rats. METHODS Collagenase-induced ICH rats were used. Inducible nitric oxide synthase(iNOS) activity of ischemic cerebral cortex

Treatment of ammonia intoxication in rats with urea cycle amino acids, furosemide and fluids.

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Three hundred sixty-seven male Wistar rats were used to compare the efficiency of urea cycle amino acids (arginine, citrulline and ornithine; Group O), furosemide (Group F), and fluid therapy (saline solution; Group FT) to treat ammonia toxicity. Rats were injected ip initially with an ammonium

Induction of myocardial nitric oxide synthase by cardiac allograft rejection.

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Cardiac transplantation, effective therapy for end-stage heart failure, is frequently complicated by allograft rejection, the mechanisms of which remain incompletely understood. Nitric oxide (NO), a vasodilator which is cytotoxic and negatively inotropic, can be produced in large amounts by an

Nitric oxide as a mediator of oxidant lung injury due to paraquat.

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At low concentrations, nitric oxide is a physiological transmitter, but in excessive concentrations it may cause cell and tissue injury. We report that in acute oxidant injury induced by the herbicide paraquat in isolated guinea pig lungs, nitric oxide synthesis was markedly stimulated, as evidenced

[Treatment and Pathomechanism of Citrin Deficiency].

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Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver. Citrin deficiency causes neonatal intrahepatic cholestasis (NICCD), which usually resolves within the first year of life. However, a small number of adults with

[Adult-onset citrullinemia].

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Adult-onset citrullinemia (CTLN2) is a rare hereditary metabolic disorder characterized by highly increased concentration of citrulline and ammonia in the plasma, which is ascribed to a deficiency of argininosuccinate synthetase (ASS), one of the urea cycle enzymes mainly located in the liver.

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