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Leht 1 alates 716 tulemused
Activation of hypoxia-inducible factor -1α via succinate dehydrogenase pathway during acute lung injury induced by trauma/hemorrhagic shock.
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Hypoxia-inducible factor (HIF)-1α is a transcription factor that is critical for tissue adaption to hypoxia and inflammation. Previous studies had indicated that normoxic activation of HIF-1α in cancer involves inhibition or mutation of the metabolic enzyme succinate dehydrogenase (SDH). We have
A role for succinate dehydrogenase genes in low chemoresponsiveness to hypoxia?
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The detection of hypoxia by the carotid bodies elicits a ventilatory response of utmost importance for tolerance to high altitude. Germline mutations in three genes encoding subunit B, C and D of succinate dehydrogenase (SDHB, SDHC and SDHD) have been associated with paragangliomas of the carotid
[Species-specific reactions of succinate dehydrogenase of lymphocytes in animals to acute hypoxic hypoxia and its relation to the radiation resistance of the body].
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Experiments on rats and dogs showed that acute hypoxic hypoxia caused an increase of succinate dehydrogenase (SDH) in blood lymphocytes. The rate of SDH increase (VSDH) depended on the oxygen concentration in the breathing hypoxic mixture (BHM) and the animal species. In dogs it proved to be lower
Clinical significance and peculiarities of succinate dehydrogenase B and hypoxia inducible factor 1α expression in parasympathetic versus sympathetic paragangliomas.
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Mitochondrial complex I, aconitase, and succinate dehydrogenase during hypoxia-reoxygenation: modulation of enzyme activities by MnSOD.
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Both NADH dehydrogenase (complex I) and aconitase are inactivated partially in vitro by superoxide (O2-.) and other oxidants that cause loss of iron from enzyme cubane (4Fe-4S) centers. We tested whether hypoxia-reoxygenation (H-R) by itself would decrease lung epithelial cell NADH dehydrogenase,
[The effect of sodium alpha-glutarate on enzymatic transamination activity and on succinate dehydrogenase in rats with different resistances to hypoxia].
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It have been found that intraperitoneal alpha-ketoglutarate injection (20 mg/100 g body weight) results in increase in the influence of cholinergic regulation mechanisms. It also results in increase of aminotransferase activity on background of the decrease of succinate dehydrogenase activity in
A novel ferulic acid derivative attenuates myocardial cell hypoxia reoxygenation injury through a succinate dehydrogenase dependent antioxidant mechanism.
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The molecular structure optimization aimed at definite target is expected to improve its anti-myocardial ischemia reperfusion (I/R) injury. Ferulic acid derivatives could probably attenuate myocardial I/R injury when optimized on account of definite target succinate dehydrogenase (SDH). Herein, an
Serum succinate by capillary zone electrophoresis: marker candidate for hypoxia.
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Serum succinate may offer an alternate analyte to lactate for the evaluation of hypoxia. To evaluate the potential uses of succinate, a relatively rapid capillary zone electrophoresis assay was developed for use in the clinical laboratory setting. Employing a simple indirect ultraviolet detection
Mycoplasma infection and hypoxia initiate succinate accumulation and release in the VM-M3 cancer cells.
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Succinate is known to act as an inflammatory signal in classically activated macrophages through stabilization of HIF-1α leading to IL-1β production. Relevant to this, hypoxia is known to drive succinate accumulation and release into the extracellular milieu. The metabolic alterations associated
[Effect of research conditions on succinate oxidation in brain mitochondria in circulatory hypoxia].
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The purpose of the study was to examine the pattern of changes revealed in the metabolic reactions in the cerebral mitochondria, oxidizing succinates in acute circulatory hypoxia under the influence of hyper- and normoxic conditions of an experiment. Following 3.5 hours of acute circulatory hypoxia
[Anaerobic formation of succinate and facilitation of its oxidation -- possible mechanisms of cell adaptation to oxygen deficiency].
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An important role of anaerobic formation of succinate in anoxic and hypoxic states and the activation of succinate oxidation under hypoxia were shown. It was concluded that, for maintaining the energetics of animal cells under conditions of oxygen deficiency, it is advisable to use substrates
Liver and heart mitochondrial succinate dehydrogenase activity of newborn rats in anoxic hypoxia and starvation.
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Succinate dehydrogenase activity was determined in the liver and heart of newborn rats after 3 and 48 hours' exposure to anoxic hypoxia (10% O2) and after 48 hours' starvation. Control determinations were made on newborn animals of corresponding ages, full term foetuses (21 days), infantile (1 and 2
Multifunctional essentiality of succinate metabolism in adaptation to hypoxia in Mycobacterium tuberculosis.
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Mycobacterium tuberculosis is a chronic, facultative intracellular pathogen that spends the majority of its decades-long life cycle in a non- or slowly replicating state. However, the bacterium remains poised to resume replicating so that it can transmit itself to a new host. Knowledge of the
Differences in the Anaerobic Lactate-Succinate Production and in the Changes of Cell Sap pH for Plants with High and Low Resistance to Anoxia.
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Anaerobically treated seedlings of Oryza sativa L. var arborio accumulated in their shoots more succinate than lactate and cell sap became alkaline. Conversely, in Triticum aestivum L. var MEK 86 lactate accumulation was far higher than that of succinate and cell sap was acidified. Anoxia clearly
Targeting mitochondria by α-tocopheryl succinate overcomes hypoxia-mediated tumor cell resistance to treatment.
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Rapidly proliferating tumor cells easily become hypoxic. This results in acquired stability towards treatment with anticancer drugs. Here, we show that cells grown at 0.1 % oxygen are more resistant towards treatment with the conventionally used anticancer drugs doxorubicin and cisplatin. The
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