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glucose 6 phosphate dehydrogenase/hypoxie
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[The effect of hypoxia on the glucose-6-phosphate dehydrogenase activity of the erythrocytes in rats].
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Biochemical methods have shown, that adaptation of rats to the conditions of the middle mountains (2100 m above sea level) as well as with subsequent affecting acute hypoxia in the hypobaric chamber (7500 m, 2-5 h and 9000 m, 1-3 h) is accompanied by the increase of the activity of
[Effect of hypoxia on activity of glucose-6-phosphate dehydrogenase in red mullet and sea scorpion tissues].
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90 min hypoxia (50% initial saturation) does not change the level of glucose-6-phosphate dehydrogenase activity in liver and brain of the red mullet. It is shown, that existence of the sea scorpion in environmental with low oxygen concentration (15% initial saturation) results in the increasing in
[Glucose-6-phosphate dehydrogenase activity in rat serum in hyperoxia, hypoxia, and cooling].
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Activity of glucose-6-phosphate dehydrogenase (G6PD) was increased in blood serum in hypoxic hypoxia, hypoxia and cooling stress. The degree of this alteration depended on duration of the action of the effectors and on oxygen pressure. Adaptation to cooling was characterized by stabilization of
Induction of the glucose-6-phosphate dehydrogenase gene expression by chronic hypoxia in PC12 cells.
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We studied the regulation of glucose-6-phosphate dehydrogenase (G6PD) gene expression by chronic hypoxia. G6PD mRNA level and activity were increased in PC12 cells by hypoxia in a dose- and time-dependent manner. Cobalt chloride and dimethyloxalylglycine, which can mimic hypoxia, also activated G6PD
Glucose-6-phosphate dehydrogenase regulation in the hepatopancreas of the anoxia-tolerant marine mollusc, Littorina littorea.
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Glucose-6-phosphate dehydrogenase (G6PDH) gates flux through the pentose phosphate pathway and is key to cellular antioxidant defense due to its role in producing NADPH. Good antioxidant defenses are crucial for anoxia-tolerant organisms that experience wide variations in oxygen availability. The
Glucose-6-Phosphate Dehydrogenase Regulation in Anoxia Tolerance of the Freshwater Crayfish Orconectes virilis.
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Glucose-6-phosphate dehydrogenase (G6PDH), the enzyme which catalyzes the rate determining step of the pentose phosphate pathway (PPP), controls the production of nucleotide precursor molecules (R5P) and powerful reducing molecules (NADPH) that support multiple biosynthetic functions, including
Glucose-6-phosphate dehydrogenase plays a critical role in hypoxia-induced CD133+ progenitor cells self-renewal and stimulates their accumulation in the lungs of pulmonary hypertensive rats.
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Although hypoxia is detrimental to most cell types, it aids survival of progenitor cells and is associated with diseases like cancer and pulmonary hypertension in humans. Therefore, understanding the underlying mechanisms that promote survival of progenitor cells in hypoxia and then developing novel
Hypoxia-induced glucose-6-phosphate dehydrogenase overexpression and -activation in pulmonary artery smooth muscle cells: implication in pulmonary hypertension.
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Severe pulmonary hypertension is a debilitating disease with an alarmingly low 5-yr life expectancy. Hypoxia, one of the causes of pulmonary hypertension, elicits constriction and remodeling of the pulmonary arteries. We now know that pulmonary arterial remodeling is a consequence of hyperplasia and
[Changes in the activity of glucose-6-phosphate dehydrogenase in the myocardium of rats with high and low resistance to hypoxia after administration of a cardiotoxic dose of epinephrine].
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[Effect of insulin and hydrocortisone on hexokinase and glucose-6-phosphate dehydrogenase activity in rat testis in conditions of chronic hypoxia].
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[The effect of insulin and hydrocortisone on hexokinase and glucose-6-phosphate dehydrogenase activity in the testes of rats under acute hypoxia].
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[Glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activity in arsenic poisoning and in hypoxemia caused by sodium nitrite].
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Glucose is necessary for stabilization of hypoxia-inducible factor-1alpha under hypoxia: contribution of the pentose phosphate pathway to this stabilization.
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In this study, we observed that low glucose or fructose reduces the increase in hypoxia-inducible factor-1alpha (HIF-1alpha) protein under hypoxic conditions. 6-Aminonicotinamide (6-AN), an inhibitor of the pentose phosphate pathway (PPP), also inhibited the increase of HIF-1alpha protein under
Icariin increases chondrocyte vitality by promoting hypoxia-inducible factor-1α expression and anaerobic glycolysis.
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[Glucose-6-phosphate dehydrogenase and catalase in the erythrocytes of patients with cerebral ischemia attacks].
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The authors assessed the activity of glucose-6-phosphate dehydrogenase and catalase in 73 patients with ischaemic cerebral attacks. They compared the results with a control group of 23 patients with vertebrogenic diseases. They recorded a mild decrease of activity of the above enzymes and draw
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