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citric acid/hypoxia
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 67 Αποτελέσματα
[Content of citric acid and ATP-citrate-lyase activity in tissues of rats with different natural resistance to hypoxic hypoxia].
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A significantly lower content of citric acid and a lower ATP-citrate-lyase activity were found in the liver of rats high-resistant to hypoxia as compared to low-resistant ones under conditions of normoxia and after "lifting at a height" of 9000 m. A dependence is supposed to exist between the
Inhibition of hypoxia-inducible factor (HIF) hydroxylases by citric acid cycle intermediates: possible links between cell metabolism and stabilization of HIF.
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The stability and transcriptional activity of the hypoxia-inducible factors (HIFs) are regulated by two oxygen-dependent events that are catalyzed by three HIF prolyl 4-hydroxylases (HIF-P4Hs) and one HIF asparaginyl hydroxylase (FIH). We have studied possible links between metabolic pathways and
Which way does the citric acid cycle turn during hypoxia? The critical role of α-ketoglutarate dehydrogenase complex.
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The citric acid cycle forms a major metabolic hub and as such it is involved in many disease states involving energetic imbalance. In spite of the fact that it is being branded as a "cycle", during hypoxia, when the electron transport chain does not oxidize reducing equivalents, segments of this
Mitochondrial dysfunction during hypoxia/reoxygenation and its correction by anaerobic metabolism of citric acid cycle intermediates.
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Kidney proximal tubule cells developed severe energy deficits during hypoxia/reoxygenation not attributable to cellular disruption, lack of purine precursors, the mitochondrial permeability transition, or loss of cytochrome c. Reoxygenated cells showed decreased respiration with complex I
Citric acid metabolism in acute anoxia in dogs.
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Tissue citric acid and susceptibility to infection in mice duringchronic hypoxia and fluoroacetate poisoning.
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[Mechanisms regulating citric acid metabolism in the brain].
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The changes in the rates of citrate biosynthesis and utilization in rat brain, liver, kidney and heart, produced by hypoxia, action of 2,4-DNP and thyreotoxicosis, were compared with changes of some regulatory parameters under the same conditions. The comparison of citrate-synthase activities,
Effect of D- and L-1,3-butanediol isomers on glycolytic and citric acid cycle intermediates in the rat brain.
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DL-1,3-butanediol (DL-BD) is an ethanol dimer which affords cerebral protection in various experimental models of hypoxia and ischemia but its mechanism of action is unknown. DL-BD is a ketogenic alcohol and it has been proposed that its protective effect was accomplished through cerebral
Proteomic analysis of the mouse brain after repetitive exposure to hypoxia.
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Hypoxic preconditioning (HPC) is known to have a protective effect against hypoxic damage; however, the precise mechanisms involved remain unknown. In this study, an acute and repetitive hypoxia mouse model, two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with
Substrate modulation of fatty acid effects on energization and respiration of kidney proximal tubules during hypoxia/reoxygenation.
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Kidney proximal tubules subjected to hypoxia/reoxygenation develop a nonesterified fatty acid-induced energetic deficit characterized by persistent partial mitochondrial deenergization that can be prevented and reversed by citric acid cycle substrates. To further assess the role of competition
Short-term treatment with glucosamine hydrochloride specifically downregulates hypoxia-inducible factor-1α at the protein level in YD-8 human tongue cancer cells.
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Hypoxia-inducible factor-1 (HIF-1) is a tumor angiogenic transcription factor composed of an α and β subunit. We investigated the effect of glucosamine hydrochloride (GS-HCl) on the expression of HIF-1α and HIF-1β in serum‑treated YD-8 human tongue cancer cells. While long-term (24 h) treatment with
Hypobaric hypoxia and hedonic matrix in rats.
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This study was carried out to evaluate the effect of continuous exposure to hypobaric hypoxia on the feeding behavior and taste responses of rats, under simulated conditions of a high altitude (HA) of 7,620 m for 21 h a day and consecutively for 18 d, which more closely resembles actual field
Effect of high-altitude hypoxia on feeding responses and hedonic matrix in rats.
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Albino male rats (n = 78) were exposed to a simulated high altitude (HA) equivalent to 7,620 m for 6 h daily, contiguously for a period of 21 days, to study their feeding behavior and gustatory responses. Their food, water intake, and body weight were recorded daily, and blood sugar and blood
Effects of hypoxia of 10-45 seconds duration on energy metabolism in the cerebral cortex of unanesthetized and anesthetized rats.
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Glycolytic and citric acid cycle intermediates, as well as organic phosphates, were measured in the cerebral cortex of unanesthetized rats following arterial hypoxia (administration of 6-8% O2) of 10 and 20 s duration. There were decreases in glucose-6-phosphate and fructose-6-phosphate, and
The citric acid cough threshold and the ventilatory response to carbon dioxide on ascent to high altitude.
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Ventilatory control undergoes profound changes on ascent to high altitude. We hypothesized that the fall in citric acid cough threshold seen on ascent to altitude is mediated by changes in the central control of cough and would parallel changes in central ventilatory control assessed by the
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