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13 Ergebnisse
Effect of postnatal hypoxia on ammonia metabolism during the early neonatal period in the rat.
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The effect of experimental hypoxia on blood glutamine, glutamate, urea, ammonia, allantoin, hypoxanthine, xanthine, urate, orotate and lactate concentrations and on PO2, PCO2 and pH in term delivered newborn rats during the first 4 h after delivery were studied. Hypoxia increased blood glutamine,
Biochemical measurement of neonatal hypoxia.
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Neonatal hypoxia ischemia is characterized by inadequate blood perfusion of a tissue or a systemic lack of oxygen. This condition is thought to cause/exacerbate well documented neonatal disorders including neurological impairment. Decreased adenosine triphosphate production occurs due to a lack of
Catabolism of cytoplasmic and intramitochondrial adenine nucleotides in C2C12 skeletal myotube under chemical hypoxia.
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Loss of adenosine-5'-triphosphate (ATP) and accumulation of inosine-5'-monophosphate (IMP) are the major purine metabolic changes in the skeletal muscle during hypoxia. This study addressed whether chemical metabolic inhibition reflects those changes in cultured skeletal myotube. For this aim,
Anti-hypoxia activity and related components of Rhodobryum giganteum par.
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Different extracts of Rhodobryum giganteum Par. were screened with mice model of acute myocardial hypoxia induced by isoproterenol and pituitrin, eight compounds, i.e. p-hydroxycinnamic acid, caffeic acid-4-O-β-d-glucopyranoside, salicin, 7,8-dihydroxy coumarin, menthol, allantoin, palmitic acid,
Hypoxanthine, uric acid and allantoin as indicators of in vivo free radical reactions. Description of a HPLC method and human brain microdialysis data.
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A practical one-step high performance liquid chromatography (HPLC) method was developed for the simultaneous determination of hypoxanthine, uric acid and allantoin in small (4 microL) microdialysis samples. The rationale for this work was the current interest in hypoxanthine as a marker for energy
Metabonomic profiling of chronic intermittent hypoxia in a mouse model.
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Chronic intermittent hypoxia (ChIH) is a dominant feature of obstructive sleep apnoea (OSA) and is associated to metabolic alterations and oxidative stress (OS). Although management of OSA is well established, the research of new biomarkers that are independent of confounding factors remains
Effects of hypoxia on the oxygen-dependent metabolism of prostaglandins and adenosine in liver cells.
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In this study, the capacity of hepatocytes to degrade prostaglandins diminished if the partial oxygen pressure dropped below 5%. This decrease was accompanied by an increased lactate/pyruvate ratio, a decrease in fatty acid oxidation and a drop in the ATP level. The degradation of exogenous
Urate produced during hypoxia protects heart proteins from peroxynitrite-mediated protein nitration.
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Tyrosine nitration is a common modification to proteins in vivo, but the reactive nitrogen species responsible for nitration are often studied in vitro using just the amino acid tyrosine in simple phosphate solutions. To investigate which reactive nitrogen species could nitrate proteins in a complex
Metabolism of hypoxanthine in isolated rat hepatocytes.
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The hepatic metabolism of hypoxanthine was investigated by studying both the fate of labelled hypoxanthine, added at micromolar concentrations to isolated rat hepatocyte suspensions, and the kinetic properties of purified hypoxanthine/guanine phosphoribosyltransferase from rat liver. More than 80%
Kinetic analysis of anaerobic metabolism in rats during acute cyanide poisoning.
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In order to investigate the changes in energy metabolism during acute anoxia, blood levels of various metabolites were analysed in cyanide-poisoned rats. After intraperitoneal injection of a sublethal dose of potassium cyanide (5 mg/kg), blood samples were obtained by cervical dislocation at
Pathways and control of adenine nucleotide catabolism in anoxic rat hepatocytes.
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Studies are reviewed that show that in isolated rat hepatocytes subjected to anoxia, the catabolism of AMP, leading to uric acid instead of to allantoin in normoxia, proceeds almost exclusively by deamination of AMP followed by dephosphorylation of IMP. Adenosine, which is nearly undetectable in
Urate oxidase in prevention and treatment of hyperuricemia associated with lymphoid malignancies.
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Standard prophylaxis and treatment of malignancy-associated hyperuricemia in the USA has been allopurinol with vigorous hydration, urinary alkalinization and osmotic diuresis. Urate oxidase, the enzyme that converts uric acid to allantoin (a readily excreted metabolite that has 5- to 10-fold higher
Bronchopulmonary dysplasia and oxidative stress: are we closer to an understanding of the pathogenesis of BPD?
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In recent years a body of data has accumulated, linking the development of bronchopulmonary dysplasia (BPD) to increased oxidative stress in the first few days after birth, since high concentrations of metabolites reflecting increased peroxidation products such as pentane, ethane, protein carbonyl,
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