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Sayfa 1 itibaren 468 Sonuçlar
Induction of macrophage glutamine: fructose-6-phosphate amidotransferase expression by hypoxia and by picolinic acid.
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We studied the expression of glutamine: fructose-6-phosphate amidotransferase (GFAT), the rate limiting enzyme in the hexosamine biosynthetic pathway controlling protein glycosylation. We obtained the first evidence that the GFAT mRNA and protein are constitutively expressed in murine mononuclear
Glutamate, glutamine and glutamine synthetase in the neonatal rat brain following hypoxia.
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Exposing 7-day-old rat pups to hypoxia, 8% oxygen/92% nitrogen, for 3 h alters glutamate (GLU), glutamine and glutamine synthetase (GS) activity in the striatum, frontal cortex and hippocampus. Immediately following the hypoxic insult there is a rapid transient elevation of GLU followed by a fall
Glutamine and glutamate limit the shortening of action potential duration in anoxia-challenged rabbit hearts.
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In clinical conditions, amino acid supplementation is applied to improve contractile function, minimize ischemia/reperfusion injury, and facilitate postoperative recovery. It has been shown that glutamine enhances myocardial ATP/APD (action potential duration) and glutathione/oxidized glutathione
Insulin receptor, IRS1, IRS2, INSIG1, INSIG2, RRAD, and BAIAP2 gene expressions in glioma U87 cells with ERN1 loss of function: effect of hypoxia and glutamine or glucose deprivation.
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OBJECTIVE
The purpose of this study was to examine: 1) the association between the expression of the insulin receptor (INSR), insulin receptor substrate 1 (IRS1) and 2 (IRS2), insulin inducible gene 1 (INSIG1) and 2 (INSIG2), Ras-related associated with diabetes (RRAD), and brain-specific
Increased glutamate uptake and glutamine synthetase activity in neuronal cell cultures surviving chronic hypoxia.
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To examine the neurochemical effects of chronic hypoxia on immature nervous tissue in vitro, mixed neuronal-glial cell cultures derived from fetal mice were exposed to 5% O2 for 24 or 48 h. Those cultures subjected to longer hypoxia manifested improved neuronal survival compared to those with the
Rapid loss of glutamine synthetase from astrocytes in response to hypoxia: implications for excitotoxicity.
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We have examined brains of neonatal pigs that were rendered hypoxic. Glutamine synthetase (GS), a key enzyme in the detoxification of glutamate and ammonia, was rapidly lost from astrocytes in regions susceptible to damage, including the CA1 of hippocampus and various cortical regions. Conversely,
[Effect of L-alanyl-L-glutamine on expression of insulin-like growth factor-1 in intestinal tissues of low-birth-weight newborn rats with hypoxia/reoxygenation-induced intestinal injury].
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OBJECTIVE
To study the effect of L-alanyl-L-glutamine (Ala-Gln) on the levels of insulin-like growth factor-1 (IGF-1) and IGF-1 receptor (IGF-1R) in the intestinal tissues of low-birth-weight (LBW) newborn rats with hypoxia/reoxygenation-induced intestinal injury.
METHODS
Pregnant rats were fed with
Effect of low glutamine/glucose on hypoxia-induced elevation of hypoxia-inducible factor-1alpha in human pancreatic cancer MiaPaCa-2 and human prostatic cancer DU-145 cells.
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OBJECTIVE
Tumor microenvironment is characterized by regions of fluctuating and chronic hypoxia, low extracellular pH, and nutrient depletion. Although it is well known that hypoxia stimulates the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha), the role of low extracellular pH and
Influence of Serum and Hypoxia on Incorporation of [(14)C]-D-Glucose or [(14)C]-L-Glutamine into Lipids and Lactate in Murine Glioblastoma Cells.
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Glucose and glutamine are essential energy metabolites for brain tumor growth and survival under both normoxic and hypoxic conditions. Both metabolites can contribute their carbons to lipid biosynthesis. We used uniformly labeled [(14)C]-U-D-glucose and [(14)C]-U-L-glutamine to examine the profile
Glutamine synthetase, glutaminase and phosphodiesterase activities in brain under hypoxia: in vitro effect of cortisol, GABA and serotonin on glutamine synthetase.
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The effect of hypobaric hypoxia on the activities of glutamine synthetase, glutaminase and cyclic 3'5' AMP phosphodiesterase in rat brain was studied after exposure to 25,000' for 6 h. Glutamine synthetase activity was increased in all the regions of brain studied, and addition of gamma amino
Hypoxia/reoxygenation impairs glucose absorption and cAMP-mediated secretion more profoundly than glutamine absorption and Ca2+/PKC-mediated secretion in rat ileum in vitro.
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BACKGROUND
Intestinal ischemia and reperfusion may lead to profuse secretion of water and electrolytes. The underlying mechanisms have been related to increased hydrostatic pressure, to denudation of intestinal villi, and, recently, to adenosine-mediated enhancement of chloride secretion.
METHODS
We
Effects of carbohydrate and glutamine supplementation on cytokine production by monocytes after exercise in hypoxia: A crossover, randomized, double-blind pilot study.
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Cerebellar glutamine synthetase in children after hypoxia or ischemia.
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BACKGROUND
Glutamate has been implicated in the pathophysiology of acute hypoxic-ischemic encephalopathy. Glutamine synthetase is an enzyme found in astrocytes that converts glutamate to its nontoxic analogue, glutamine. The present study tests the hypothesis that brain glutamine synthetase activity
Nitric oxide (no), citrulline - no cycle enzymes, glutamine synthetase and oxidative stress in anoxia (hypobaric hypoxia) and reperfusion in rat brain.
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Nitric oxide is postulated to be involved in the pathophysiology of neurological disorders due to hypoxia/ anoxia in brain due to increased release of glutamate and activation of N-methyl-D-aspartate receptors. Reactive oxygen species have been implicated in pathophysiology of many neurological
Glutamine protects neuronal function against cerebral hypoxia: a study using the in vitro hippocampal slice preparation.
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Pretreatment of hippocampal slices with glutamine doubled the recovery rate of the synaptic function (electrically evoked population spike) from a standardized hypoxic insult in CA1 pyramidal neurons. This protective effect of glutamine was dose-dependent and biphasic; recovery of synaptic function
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