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Sida 1 från 129 resultat
Permeability transition pore-dependent and PARP-mediated depletion of neuronal pyridine nucleotides during anoxia and glucose deprivation.
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Exposure of rat cortical neurons to combined oxygen and glucose deprivation results in loss of NAD(P)H autofluorescence that is only partially reversible following restoration of oxygen and glucose, suggesting catabolism of pyridine nucleotides. This study tested the hypothesis that metabolic
[Pyridine nucleotide content in the brain and myocardium of rats under combined effect of hypercapnia, hypoxia and cooling].
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In experiments with rats, subjected to single and repeated simultaneous effect of hypercapnia, hypoxia and cooling, contents of pyridine nucleotides (NAD, NADP, NAD-H2 and NADP-H2) and macroergic substances were studied and also the activity of dehydrogenases of the pentose pathway was determined in
Pyridine nucleotides of rabbit cornea with histotoxic anoxia: chemical analysis, non-invasive fluorometry and physiological correlates.
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The pyridine nucleotides from both the epithelium and the endothelium of rabbit cornea were measured by the cycling assay. Sodium azide (10 mM) applied for 1 hr to induce histotoxic anoxia decreased the endothelial NAD+/NADH ratio from 4.62 to 1.49 and decreased the epithelial NAD+/NADH ratio from
Reductive metabolism of the hypoxia marker pimonidazole is regulated by oxygen tension independent of the pyridine nucleotide redox state.
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2-Nitroimidazoles, such as pimonidazole, are reduced in cells with low oxygen tension and are, therefore, used as hypoxia markers. However, the effect of the pyridine nucleotide redox state on pimonidazole reduction is not known. Therefore, livers from fed or fasted rats were perfused with
Periportal and pericentral pyridine nucleotide fluorescence from the surface of the perfused liver: evaluation of the hypothesis that chronic treatment with ethanol produces pericentral hypoxia.
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Pyridine nucleotide fluorescence made from the surface of the hemoglobin-free perfused rat liver was measured continuously by using a "micro-light guide" placed on selected periportal and pericentral regions of the liver lobule. From the portal oxygen tension at which pyridine nucleotide reduction
Anoxia-induced changes in pyridine nucleotide redox state in cortical neurons and astrocytes.
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NAD(P)H autofluorescence was used to verify establishment of metabolic anoxia using primary cultures of cortical neurons and astrocytes. Cells on cover slips were placed in a chamber and O(2) was displaced by continuous infusion of argon. Perfusion with medium at PO(2) < 0.4 mm Hg caused an increase
Studies of mechanisms of chemical radiation protection in vivo. 3. Changes in fluorescence of intracellular pyridine nucleotides and modification by extracellular hypoxia.
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Flavin and pyridine nucleotide oxidation-reduction changes in perfused rat liver. I. Anoxia and subcellular localization of fluorescent flavoproteins.
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Correlation of oxidation-reduction changes of intracellular reduced pyridine nucleotide and changes in electroencephalogram of the rat in anoxia.
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[Effect of certain water-soluble vitamins on the pyridine coenzyme content of animal tissues under conditions of hypoxia].
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[Content of pyridine nucleotides and some metabolites in rat kidney cortex during normal oxygen tension and anoxia].
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Selective modulation of membrane currents by hypoxia in intact airway chemoreceptors from neonatal rabbit.
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1. We previously described voltage-dependent ionic currents and hypoxia chemosensitivity in cultured pulmonary neuroepithelial body (NEB) cells isolated from fetal rabbit. Here we use fresh neonatal rabbit lung slices (200-400 micrometer thick) to characterize the electrophysiological properties of
Structural basis for binding of cyclic 2-oxoglutarate analogues to factor-inhibiting hypoxia-inducible factor.
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Aromatic analogues of the 2-oxoglutarate co-substrate of the hypoxia-inducible factor hydroxylases are shown to bind at the active site iron: Pyridine-2,4-dicarboxylate binds as anticipated with a single molecule chelating the iron in a bidentate manner. The binding mode of a hydroxamic acid
Pyridine nucleotide as an indicator of the oxygen requirements for energy-linked functions of mitochondria.
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The responses of cardiac mitochondria to anoxia may be evaluated in terms of the oxidation-reduction state of the electron carriers and the ability of the mitochondria to function in energy-linked reactions. The previous detailed evaluation of the oxygen requirements for electron transfer in
The influence of various precursors on the concentration of energy-rich phosphates and pyridine nucleotides in cardiac tissue and its possible meaning for anoxic survival.
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A special "anoxia test" was developed with isolated guinea pig atria to test influences on the anoxic energy balance. Adenine, ribose, nicotinic acid or nicotinamide added as precursors to nutrition solutions inhibit the loss of cardiac adenine and pyridine nucleotides during anoxia and improve the
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