ascorbic/hypoxia

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[Effect of ascorbic acid during acute iterative anoxia, hypothesis of an anti-oxidizing mechanism of action in comparison with the effect of hydroquinone].

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Some of the problems which appear during senescence, are said to be caused by cerebral oxygen deficiency and various experiments have been set up to try to imitate this particular aspect of the ageing process. We have already studied the action of many drugs with regard to acute repeated anoxia. Our

Sugar transport regulation in avian red blood cells: role of Ca2+ in the stimulatory effects of anoxia, adrenaline, and ascorbic acid.

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Membrane transport of sugar and Ca2+ was studied in pigeon erythrocytes by measuring the cell to medium distribution of 3-O-[14C]methyl-D-glucose and 45Ca. We have found that stimulation of sugar transport by anoxia, adrenaline, or ascorbic acid was not dependent on external Ca2+, nor was it

Modification of iron uptake and lipid peroxidation by hypoxia, ascorbic acid, and alpha-tocopherol in iron-loaded rat myocardial cell cultures.

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The ability of ascorbic acid, alpha-tocopherol, and hypoxia to modify iron uptake, chelation, and toxicity as manifested by the generation of malonyldialdehyde (MDA) was studied in myocardial cell cultures obtained from newborn rats. Exposure to 20 micrograms/ml iron provided as 59Fe-ferric ammonium

Electrochemical monitoring of brain ascorbic acid changes associated with hypoxia, spreading depression, and seizure activity.

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In vivo electrochemistry has been a valuable tool in detecting real time neurochemical changes in extracellular fluid. Absolute selectivity has been difficult to achieve previously, but we report here a carbon fiber electrode and measurement technique which is specific for one oxidizable species:

Ascorbic acid does not enhance hypoxia-induced vasodilation in healthy older men.

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In response to hypoxia, a net vasodilation occurs in the limb vasculature in young healthy humans and this is referred to as "hypoxia-induced vasodilation". We performed two separate experiments to determine (1) if hypoxia-induced forearm vasodilation is impaired in older men (n = 8) compared to

Ascorbic acid and alpha-tocopherol protect age-dependently from hypoxia-induced changes of cortical excitability in developing rats.

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OBJECTIVE The effects of ascorbic acid and α-tocopherol pre-treatment on hypoxia induced changes in brain cortex excitability were tested in immature rats exposed chronically to simulated altitude of 7 000 m. METHODS Rat pups were kept together with their mothers for 8 hours a day in hypobaric

[The effect of acute and chronic hypoxia on ascorbic acid levels in various areas of the brain, liver, adrenal glands and in biological fluids in 18-day-old rats].

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The influence of acute and chronic hypoxia on the ascorbic acid content in liver, adrenal, plasma, cerebrospinal fluid and brain in 18-day-old rats was studied. Due to acute hypoxia a significant decrease in ascorbic acid concentration in the adrenal occurred. Its levels in plasma and cerebrospinal

Maternal infusion of antioxidants (Trolox and ascorbic acid) protects the fetal heart in rabbit fetal hypoxia.

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The antioxidants, Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid, a water soluble analog of vitamin E) and ascorbic acid (AA), protect the heart from ischemia-reperfusion injury. We hypothesized that maternal infusion of Trolox and AA, would reduce the fetal bradycardia and

Effects of ascorbic acid supplementation on male reproductive system during exposure to hypoxia.

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Two groups of male rats were exposed to simulated altitudes of 6060 m and 7576 m for 6 h/day for 7 days (intermittent exposure). In two additional groups of animals exposed to the same altitude, 100 mg of ascorbic acid (AA) was fed daily for 5 days prior to the exposure period and also during the

Protective effect of flavonoids and tocopherol in high altitude hypoxia in the rat: comparison with ascorbic acid.

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The mixture of flavonoids (silymarin) from Carduus Marianus (0.9 mg.g-1 body weight) and/or ascorbic acid (0.4 mg.g-1 body weight) were administered in the food to 21 day-old (b.w. 35-45 g) rats for one week. Then the animals were exposed, in a hypobaric chamber, to simulated altitude 8,000-12,000 m

A carbon dot-based fluorescent nanoprobe for the associated detection of iron ions and the determination of the fluctuation of ascorbic acid induced by hypoxia in cells and in vivo.

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Maintaining the redox balance of biological systems is a key point to maintain a healthy physiological environment. Excessive iron ions (Fe3+) can cause apoptosis, tissue damage and death. Fortunately, ascorbic acid (AA) as a reducing agent has been evaluated for the reduction of Fe3+. Moreover, AA

High levels of ascorbic acid, not glutathione, in the CNS of anoxia-tolerant reptiles contrasted with levels in anoxia-intolerant species.

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Ascorbic acid and glutathione (GSH) are antioxidants and free radical scavengers that provide the first line of defense against oxidative damage in the CNS. Using HPLC with electrochemical detection, we determined tissue contents of these antioxidants in brain and spinal cord in species with varying

Exploration of effects of emodin in selected cancer cell lines: enhanced growth inhibition by ascorbic acid and regulation of LRP1 and AR under hypoxia-like conditions.

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This study explores the link between the antiproliferative activity of emodin through the generation of reactive oxygen species (ROS) in various cancer cell lines and the expression of the androgen receptor (AR) in the prostate cancer cell lines LNCaP (androgen-sensitive) and PC-3

Ascorbic acid, but not dehydroascorbic acid increases intracellular vitamin C content to decrease Hypoxia Inducible Factor -1 alpha activity and reduce malignant potential in human melanoma.

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BACKGROUND Accumulation of hypoxia inducible factor-1 alpha (HIF-1α) in malignant tissue is known to contribute to oncogenic progression and is inversely associated with patient survival. Ascorbic acid (AA) depletion in malignant tissue may contribute to aberrant normoxic activity of HIF-1α. While

Sex-dependent co-occurrence of hypoxia and β-amyloid plaques in hippocampus and entorhinal cortex is reversed by long-term treatment with ubiquinol and ascorbic acid in the 3 × Tg-AD mouse model of Alzheimer's disease.

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Structural and functional abnormalities in the cerebral microvasculature have been observed in Alzheimer's disease (AD) patients and animal models. One cause of hypoperfusion is the thickening of the cerebrovascular basement membrane (CVBM) due to increased collagen-IV deposition around capillaries.

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ascorbic/hypoxia

[Effect of ascorbic acid during acute iterative anoxia, hypothesis of an anti-oxidizing mechanism of action in comparison with the effect of hydroquinone].

Sugar transport regulation in avian red blood cells: role of Ca2+ in the stimulatory effects of anoxia, adrenaline, and ascorbic acid.

Modification of iron uptake and lipid peroxidation by hypoxia, ascorbic acid, and alpha-tocopherol in iron-loaded rat myocardial cell cultures.

Electrochemical monitoring of brain ascorbic acid changes associated with hypoxia, spreading depression, and seizure activity.

Ascorbic acid does not enhance hypoxia-induced vasodilation in healthy older men.

Ascorbic acid and alpha-tocopherol protect age-dependently from hypoxia-induced changes of cortical excitability in developing rats.

[The effect of acute and chronic hypoxia on ascorbic acid levels in various areas of the brain, liver, adrenal glands and in biological fluids in 18-day-old rats].

Maternal infusion of antioxidants (Trolox and ascorbic acid) protects the fetal heart in rabbit fetal hypoxia.

Effects of ascorbic acid supplementation on male reproductive system during exposure to hypoxia.

Protective effect of flavonoids and tocopherol in high altitude hypoxia in the rat: comparison with ascorbic acid.

A carbon dot-based fluorescent nanoprobe for the associated detection of iron ions and the determination of the fluctuation of ascorbic acid induced by hypoxia in cells and in vivo.

High levels of ascorbic acid, not glutathione, in the CNS of anoxia-tolerant reptiles contrasted with levels in anoxia-intolerant species.

Exploration of effects of emodin in selected cancer cell lines: enhanced growth inhibition by ascorbic acid and regulation of LRP1 and AR under hypoxia-like conditions.

Ascorbic acid, but not dehydroascorbic acid increases intracellular vitamin C content to decrease Hypoxia Inducible Factor -1 alpha activity and reduce malignant potential in human melanoma.

Sex-dependent co-occurrence of hypoxia and β-amyloid plaques in hippocampus and entorhinal cortex is reversed by long-term treatment with ubiquinol and ascorbic acid in the 3 × Tg-AD mouse model of Alzheimer's disease.

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Sex-dependent co-occurrence of hypoxia and β-amyloid plaques in hippocampus and entorhinal cortex is reversed by long-term treatment with ubiquinol and ascorbic acid in the 3 × Tg-AD mouse model of Alzheimer's disease.