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Σελίδα 1 από 236 Αποτελέσματα
Hypoxia depletes ascorbate in the cat carotid body.
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Vitamin C or L-ascorbate is an effective endogenous reducing agent influencing the functions that are involved with the redox mechanism. Detection of oxygen tension changes by the carotid body chemoreceptors is one such function. In this study we investigated the hypothesis that the level of
Seasonal- and temperature-dependent variation in CNS ascorbate and glutathione levels in anoxia-tolerant turtles.
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We determined the ascorbic acid (ascorbate) and glutathione (GSH) contents of eight regions of the CNS from anoxia-tolerant turtles collected in summer and in winter. Ascorbate was of special interest because it is found in exceptionally high levels in the turtle CNS. The temperature-dependence of
Stimulation of ascorbate-induced hypoxia by lignin.
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Alkali-lignin, lignin sulfonate or protein-bound polysaccharide (PSK) significantly enhanced the ascorbyl radical intensity and cytotoxic activity of ascorbate, but inhibited the intracellular incorporation of [14C]ascorbic acid. These natural products also enhanced ascorbate-induced oxygen
4-O-Methylascochlorin inhibits the prolyl hydroxylation of hypoxia-inducible factor-1α, which is attenuated by ascorbate.
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4-O-Methylascochlorin (MAC), a methylated derivative of ascochlorin, was previously shown to promote the accumulation of hypoxia-inducible factor (HIF)-1α in human breast adenocarcinoma MCF-7 cells. In the present study, we further investigated the effects of MAC on the expression and function of
Response of the ascorbate-glutathione cycle to re-aeration following hypoxia in lupine roots.
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The response of the enzymes and metabolites of the ascorbate-glutathione pathway to oxidative stress caused by re-aeration following hypoxia was studied in roots of hydroponically grown lupine (Lupinus luteus L. cv. Juno) seedlings. Lupine roots were deprived of oxygen by subjecting them to hypoxia
Consequences of hypoxia on the cell size of neuropeptide-Y neurons and the role of ascorbate in cultured neurons from chick embryo.
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The effect of ascorbate on the cell size of neuropeptide-Y neurons (NPY) and ascorbate uptake was studied in hypoxic neuronal cultures from chick embryo. Primary neuronal cultures plated on coverslips or on plastic dishes were switched to the serum free or serum supplemented medium and exposed to
Effect of acute hypoxia on ascorbate content of plasma, cerebral cortex, and adrenal gland.
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Levels of ascorbic acid (AA) in the plasma, brain, and adrenal gland of rats were determined after 15 min of hypoxia (PaO2 less than 25 mm Hg) and following asphyxia. In rabbits, AA plasma levels were followed up to 75 min of reoxygenation following 15 min of hypoxia of the same severity. A
Gulonolactone Addition to Human Hepatocellular Carcinoma Cells with Gene Transfer of Gulonolactone Oxidase Restores Ascorbate Biosynthesis and Reduces Hypoxia Inducible Factor 1.
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Humans are unable to synthesise ascorbate (Vitamin C) due to the lack of a functional gulonolactone oxidase (Gulo), the enzyme that catalyses the final step in the biosynthesis pathway. Ascorbate is a vital micronutrient required for many biological functions, including as a cofactor for
Hypoxia-inducible factor-1alpha stabilization in nonhypoxic conditions: role of oxidation and intracellular ascorbate depletion.
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Hypoxia-inducible factor-1 (HIF-1) is a decisive element for the transcriptional regulation of many genes induced under low oxygen conditions. Under normal oxygen conditions, HIF-1alpha, the active subunit of HIF-1, is hydroxylated on proline residues by specific HIF prolyl-hydroxylases, leading to
Ascorbate depletion mediates up-regulation of hypoxia-associated proteins by cell density and nickel.
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Exposure of human lung cells to carcinogenic nickel compounds in the presence of oxygen up-regulated carbonic anhydrase IX (CA IX) and NDRG1/Cap43, both known as intrinsic hypoxia markers and cancer-associated genes. This suggests that factors other than a shortage of oxygen may be involved in this
Effects of transferrin receptor blockade on cancer cell proliferation and hypoxia-inducible factor function and their differential regulation by ascorbate.
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Cellular iron is needed for cell survival and hydroxylation of hypoxia-inducible factor-1alpha (HIF-alpha) by prolyl hydroxylases (PHD). One mechanism of iron uptake is mediated by the cell surface transferrin receptor (TfR). Because iron is required for cell growth and suppression of HIF-alpha
Ascorbate deficiency results in impaired neutrophil apoptosis and clearance and is associated with up-regulation of hypoxia-inducible factor 1α.
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Some cells, including neutrophils, accumulate high intracellular ascorbate concentrations, which suggests that they have an important function in these cells. In this study we have used L-gulono-γ-lactone oxidase (Gulo)-/- mice, which are unable to synthesize ascorbate, to generate
Ascorbate deficiency results in impaired neutrophil apoptosis and clearance and is associated with up-regulation of hypoxia-inducible factor 1alpha.
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Some cells, including neutrophils, accumulate high intracellular ascorbate concentrations, which suggests that they have an important function in these cells. In this study we have used L-gulono-gamma-lactone oxidase (Gulo)-/- mice, which are unable to synthesize ascorbate, to generate
The ROS-induced cytotoxicity of ascorbate is attenuated by hypoxia and HIF-1alpha in the NCI60 cancer cell lines.
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Intravenous application of high-dose ascorbate is used in complementary palliative medicine to treat cancer patients. Pharmacological doses of ascorbate in the mM range induce cytotoxicity in cancer cells mediated by reactive oxygen species (ROS), namely hydrogen peroxide and ascorbyl radicals.
Activation of the hypoxia pathway in breast cancer tissue and patient survival are inversely associated with tumor ascorbate levels.
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