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tocopherol/seizures
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[Model corasol-induced seizures are followed by increase of nitric oxide generation and are abolished by mexidol and alpha-tocopherol].
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The effect of mexidol and alpha-tocopherol on the onset and development of acute epilepsy model was studied in Wistar rats using penthylenetetrazole induced convulsions. The intensity of the nitric oxide (NO) production in the cerebral cortex was determined by a direct method using electron
Catalase and alpha-tocopherol attenuate blood-brain barrier breakdown in pentylenetetrazole-induced epileptic seizures in acute hyperglycaemic rats.
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Experimental data indicate that acute hyperglycaemia can aggravate the consequences of epileptic seizures on the permeability of the blood-brain barrier (BBB). The purpose of this study was to examine the effects of chronic administration of alpha -tocopherol (vitamin E) and acute catalase
alpha-Tocopherol protects against pentylenetetrazol- and methylmalonate-induced convulsions.
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Increased excitatory amino acid transmission and decreased GABAergic inhibitory responses seem to be important mechanisms in the genesis of convulsions, where reactive oxygen species (ROS) have recently been suggested to play a critical role. Therefore, administration of antioxidants may be
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
The effects of alpha-tocopherol on hippocampal oxidative stress prior to in pilocarpine-induced seizures.
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Reactive oxygen species have been implicated in seizure-induced neurodegeneration, and there is a correlation between free radical level and scavenger enzymatic activity in the epilepsy. It has been suggested that pilocarpine-induced seizures is mediated by an increase in oxidative stress. Current
Post-seizure α-tocopherol treatment decreases neuroinflammation and neuronal degeneration induced by status epilepticus in rat hippocampus.
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Vitamin E (as α-tocopherol, α-T) was shown to have beneficial effects in epilepsy, mainly ascribed to its antioxidant properties. Besides radical-induced neurotoxicity, neuroinflammation is also involved in the pathophysiology of epilepsy, since neuroglial activation and cytokine production
Oxidative stress in rat striatum after pilocarpine-induced seizures is diminished by alpha-tocopherol.
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Alpha-tocopherol has numerous nonenzymatic actions and is a powerful liposoluble antioxidant. The objective of the present study was to evaluate the neuroprotective effects of alpha-tocopherol in rats against oxidative stress caused by pilocarpine-induced seizures. Wistar rats were intraperitoneally
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
Neurobiological Correlates of Alpha-Tocopherol Antiepileptogenic Effects and MicroRNA Expression Modulation in a Rat Model of Kainate-Induced Seizures.
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Seizure-triggered maladaptive neural plasticity and neuroinflammation occur during the latent period as a key underlying event in epilepsy chronicization. Previously, we showed that α-tocopherol (α-T) reduces hippocampal neuroglial activation and neurodegeneration in the rat model of kainic acid
The role of superoxide dismutase and alpha-tocopherol in the development of seizures and kindling induced by pentylenetetrazol - influence of the radical scavenger alpha-phenyl-N-tert-butyl nitrone.
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Previous experiments have shown that the generation of free hydroxyl radicals in rat brain homogenates is increased following pentylenetetrazol (PTZ) kindling. The present study was performed in order to evaluate the involvement of endogeneous radical defence systems as the superoxide dismutase
Influence of systemic factors on experimental epileptic brain injury. Structural changes accompanying bicuculline-induced seizures in rats following manipulations of tissue oxygenation or alpha-tocopherol levels.
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A previous study from the laboratory showed that status epilepticus induced by bicuculline administration to ventilated rats produced astrocytic swelling and nerve cell changes ("type 1 and 2 injury") particularly in layers 3 and 5 of the neocortex (Söderfeldt et al. 1981). The type 1 injured
Vitamin E deficiency and seizures in animals and man.
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Study of 100 children with grand mal convulsive disorders and 100 medically healthy children of matching age showed significantly lower plasma levels of vitamin E in the former (means 632.2 +/- 17.3 and 822.5 +/- 21.8 micrograms/dl respectively; p less than 0.001). This finding accords with the
α-Tocopherol and Hippocampal Neural Plasticity in Physiological and Pathological Conditions.
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Neuroplasticity is an "umbrella term" referring to the complex, multifaceted physiological processes that mediate the ongoing structural and functional modifications occurring, at various time- and size-scales, in the ever-changing immature and adult brain, and that represent the basis for
A possible role of lipid peroxidation in cellular damages caused by cerebral ischemia and the protective effect of alpha-tocopherol administration.
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Incomplete global cerebral ischemia was induced by clamping the bilateral common carotid arteries of spontaneously hypertensive rats (SHR) and blood reperfusion was allowed by declamping the arteries after indicated times. To investigate the possible role of lipid peroxidation which causes
The involvement of nitric oxide in the anticonvulsant effects of alpha-tocopherol on penicillin-induced epileptiform activity in rats.
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A variety of animal seizure models exist which help to document the effects of alpha-tocopherol (Vitamin E) and specify its action. In the present study, we provide further evidence for the functional involvement of NO in the anticonvulsant effects of alpha-tocopherol on penicillin-induced
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