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succinate dehydrogenase/hypoxie
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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
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
Essentiality of succinate dehydrogenase in Mycobacterium smegmatis and its role in the generation of the membrane potential under hypoxia.
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Succinate:quinone oxidoreductase (Sdh) is a membrane-bound complex that couples the oxidation of succinate to fumarate in the cytoplasm to the reduction of quinone to quinol in the membrane. Mycobacterial species harbor genes for two putative sdh operons, but the individual roles of these two
[Comparison of changes in succinate dehydrogenase activity in blood lymphocytes and modification of radiosensitivity by exogenous hypoxia].
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Radioprotective efficiency of gas hypoxic mixtures (GHM) containing 5-12% of oxygen and the rate of the reaction of succinate dehydrogenase (VSDG) activity in peripheral blood lymphocytes upon breathing GHM were comparatively studied in rats and dogs. VSDG was 4393.5 (%O2)-2.58 and 130.76 (%O2)-1.42
Modeling succinate dehydrogenase loss disorders in C. elegans through effects on hypoxia-inducible factor.
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Mitochondrial disorders arise from defects in nuclear genes encoding enzymes of oxidative metabolism. Mutations of metabolic enzymes in somatic tissues can cause cancers due to oncometabolite accumulation. Paraganglioma and pheochromocytoma are examples, whose etiology and therapy are complicated by
Nature of the activation of succinate dehydrogenase by various effectors and in hypobaria and hypoxia.
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Modulation of succinate dehydrogenase in response to environmental stress conditions of hypobaria and hypoxia.
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Respiratory control and sternohyoid muscle structure and function in aged male rats: decreased susceptibility to chronic intermittent hypoxia.
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Obstructive sleep apnoea syndrome (OSAS) is a common respiratory disorder characterized by chronic intermittent hypoxia (CIH). We have shown that CIH causes upper airway muscle dysfunction in the rat due to oxidative stress. Ageing is an independent risk factor for the development of OSAS perhaps
Mitochondrial complex II is essential for hypoxia-induced pulmonary vasoconstriction of intra- but not of pre-acinar arteries.
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OBJECTIVE
Alveolar hypoxia acutely elicits contraction of pulmonary arteries, leading to a rise in pulmonary arterial pressure (PAP) and shifting blood to better ventilated areas of the lung. The molecular mechanisms underlying this hypoxic pulmonary vasoconstriction (HPV) are still incompletely
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