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ascorbic acid/эпилептический припадок
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Страница 1 от 56 полученные результаты
Low brain ascorbic acid increases susceptibility to seizures in mouse models of decreased brain ascorbic acid transport and Alzheimer's disease.
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Seizures are a known co-occurring symptom of Alzheimer's disease, and they can accelerate cognitive and neuropathological dysfunction. Sub-optimal vitamin C (ascorbic acid) deficiency, that is low levels that do not lead the sufferer to present with clinical signs of scurvy (e.g. lethargy,
Ascorbic acid and alpha-tocopherol attenuate methylmalonic acid-induced convulsions.
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The effects of chronic administration of alpha-tocopherol or melatonin, or acute ascorbic acid administration on the convulsant action of methylmalonic acid (MMA) were investigated in adult male rats. Animals were chronically injected with alpha-tocopherol (40 mg kg(-1), i.p.), melatonin (5 mg
Neuronal damage and memory deficits after seizures are reversed by ascorbic acid?
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The objective of the present study was to evaluate the neuroprotective effects of ascorbic acid (AA) in rats, against the neuronal damage and memory deficit caused by seizures. Wistar rats were treated with 0.9% saline (i.p., control group), ascorbic acid (500 mg/kg, i.p., AA group), pilocarpine
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:
Kainic acid causes redox changes in cerebral cortex extracellular fluid: NMDA receptor activity increases ascorbic acid whereas seizure activity increases uric acid.
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Kainic acid (KA) causes seizures and extensive brain damage in rats. To study the effects of KA on the redox state in cerebral cortex extracellular fluid (ECF), ascorbic and uric acid concentrations were measured in intracerebral microdialysis samples before and after systemic KA administration
Inhibitory action of antioxidants (ascorbic acid or alpha-tocopherol) on seizures and brain damage induced by pilocarpine in rats.
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Temporal lobe epilepsy is the most common form of epilepsy in humans. Oxidative stress is a mechanism of cell death induced by seizures. Antioxidant compounds have neuroprotective effects due to their ability to inhibit free radical production. The objectives of this work were to comparatively study
Combined Low-Intensity Exercise and Ascorbic Acid Attenuates Kainic Acid-Induced Seizure and Oxidative Stress in Mice.
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Physical exercise and vitamins such as ascorbic acid (ASC) have been recognized as an effective strategy in neuroprotection and neurorehabilitatioin. However, there is a need to find an efficient treatment regimen that includes ASC and low-intensity exercise to diminish the risk of overtraining and
Ascorbic acid ameliorates seizures and brain damage in rats through inhibiting autophagy.
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Oxidative stress is a mechanism of cell death induced by seizures. Antioxidant compounds have neuroprotective effects due to their ability to inhibit free radical production. Autophagy is a process in which cytoplasmic components such as organelles and proteins are delivered to the lysosomal
Oxidative stress in the hippocampus during experimental seizures can be ameliorated with the antioxidant ascorbic acid.
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Ascorbic acid has many nonenzymatic actions and is a powerful water-soluble antioxidant. It protects low density lipoproteins from oxidation and reduces harmful oxidants in the central nervous system. Pilocarpine-induced seizures have been suggested to be mediated by increases in oxidative stress.
Regional brain ascorbic acid distribution: its functional relationship to appetite and leptazol-induced convulsions in guinea-pigs.
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The distribution of ascorbic acid has been compared in the fore-, mid- and hind-brains of guinea-pigs maintained on a scorbutogenic diet alone, or the diet with supplementary Vitamin C, or the supplemented diet and a terminal convulsant dose of leptazol after 27 days. At the beginning of the
Proceedings: The relationship of ascorbic acid to leptazol-induced convulsions in guinea-pigs.
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The effect of audiogenic seizures in rats on the adrenal weight, ascorbic acid, cholesterol, and corticosteroids.
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Effects of ascorbate on a dopaminergic response: apomorphine-induced modification of pentylenetetrazol-induced seizures in mice.
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The threshold for pentylenetetrazol (PTZ)-induced clonic seizures is below control levels 15 min after administration of apomorphine (APO) but above them 60 min after APO administration. Pretreatment with ascorbic acid (10 mg/kg) or the presence of ascorbic acid in the APO solution (1 mg/ml)
Effect of 6-hydroxydopamine pretreatment on spontaneous convulsions induced by barbital withdrawal.
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Following withdrawal from chronic barbital administration, 6-hydroxydopamine pretreated rats show a greater number and an earlier onset of spontaneous convulsive seizures than do rats pretreated with the saline-ascorbic acid vehicle.
Dimethyl sulfoxide and ebselen prevent convulsions induced by 5-aminolevulinic acid.
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We investigated whether intrastriatal (i.s.) administration of 5-aminolevulinic acid (ALA) induces oxidative damage and whether behavioral alterations induced by i.s. administration of ALA could be affected by antioxidants. Unilateral injection of ALA (6 micromol/striatum) increased (approximately
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