glutathione/seizures

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Effects of cell phone radiation on lipid peroxidation, glutathione and nitric oxide levels in mouse brain during epileptic seizure.

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The objective of the this study was to evaluate the effects of cellular phone radiation on oxidative stress parameters and oxide levels in mouse brain during pentylenetetrazole (PTZ) induced epileptic seizure. Eight weeks old mice were used in the study. Animals were distributed in the following

The role of the glutathione system in seizures induced by diphenyl diselenide in rat pups.

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The present study investigated the role of the glutathione system in seizures induced by diphenyl diselenide (PhSe)(2) (50 mg/kg) in rat pups (post natal day, 12-14). Reduced glutathione (GSH) (300 nmol/site; i.c.v.), administered 20 min before (PhSe)(2), abolished the appearance of seizures,

Enhanced lipid peroxidation in epileptics with null genotype of glutathione S-transferase M1 and intractable seizure.

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Null genotype of glutathione S-transferase class me (GSTM1(-)) and the plasma level of malondialdehyde (MDA) were determined in normal subjects, epileptics with good seizure control and epileptics with intractable seizure. The frequency of GSTM1(-) of the epileptics with intractable seizure was

Lipoic acid increases glutathione peroxidase, Na+, K+-ATPase and acetylcholinesterase activities in rat hippocampus after pilocarpine-induced seizures?

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In the present study we investigated the effects of lipoic acid (LA) on acetylcholinesterase (AChE), glutathione peroxidase (GPx) and Na+, K+-ATPase activities in rat hippocampus during seizures. Wistar rats were treated with 0.9% saline (i.p., control group), lipoic acid (20 mg/kg, i.p., LA group),

Evaluation of glutathione metabolism in NMDA preconditioning against quinolinic acid-induced seizures in mice cerebral cortex and hippocampus.

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Brain preconditioning refers to a wide range of treatments that induce a neuronal tolerance state where neuronal tissue become more resistant to a subsequent lethal insult. The mechanisms underlying the preconditioning-induced brain tolerance are not fully understood, but up-regulation of

Lipoic acid alters delta-aminolevulinic dehydratase, glutathione peroxidase and Na+,K+-ATPase activities and glutathione-reduced levels in rat hippocampus after pilocarpine-induced seizures.

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In the present study, we investigated the effects of lipoic acid (LA) in the brain oxidative stress caused by pilocarpine-induced seizures in adult rats. Wistar rats were treated with 0.9% saline (i.p., control group), lipoic acid (10 mg/kg, i.p., LA group), pilocarpine (400 mg/kg, i.p., pilocarpine

Feasible Relation between Glutathione Peroxidase and Febrile Seizure.

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OBJECTIVE We aimed to determine the relationship between serum glutathione peroxidase and febrile seizure. METHODS In this case-control study, 43 children with simple febrile seizure (case group) were compared with 43 febrile children without seizure (control group) in terms of serum glutathione

Reduced and oxidized glutathione in brain and convulsions.

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Concentration changes of reduced glutathione (GSH) and oxidized glutathione (GSSG) were studied by fluorometric assay with omicron-phthalaldehyde to clarify the relationship between seizure mechanism and the glutathione redox state. In cerebellum the GSH/GSSG ratio was significantly decreased in the

Chronic brain oxidation in a glutathione peroxidase knockout mouse model results in increased resistance to induced epileptic seizures.

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Systemic administration of kainic acid (KA) to rodents results in limbic seizures and subsequent neurodegeneration similar to that observed in certain types of human epilepsy, and it is a commonly used animal model for this disease. Oxidative stress has been suggested to play a role in the neuronal

Increased susceptibility of glutathione peroxidase-1 transgenic mice to kainic acid-related seizure activity and hippocampal neuronal cell death.

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Glutathione peroxidase (GSHPx) has been demonstrated in several in vivo studies to reduce both the risk and severity of oxidatively-induced tissue damage. The seizure-inducing neurotoxin kainic acid (KA) has been suggested to elicit its toxic effects in part via generation of oxidative stress. In

Role of glutathione peroxidase in the ontogeny of hippocampal oxidative stress and kainate seizure sensitivity in the genetically epilepsy-prone rats.

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Oxidative stress may contribute to epileptogenicity in genetic models of epilepsy. To address this, we examined the enzymatic activity of cytosolic Cu/Zn superoxide dismutase (SOD-1), mitochondrial Mn superoxide dismutase (SOD-2), and glutathione peroxidase (GPx) in the developing hippocampus of

Glutathione peroxidase deficiency and childhood seizures.

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4 children with intractable seizures, repeated infections, and intolerance to anticonvulsants had evidence of glutathione peroxidase deficiency. 2 had low intracellular enzyme activity but normal blood selenium and high plasma glutathione peroxidase concentrations. The other 2 had low intracellular

Pentylenetetrazol-induced seizures and kindling: changes in free fatty acids, superoxide dismutase, and glutathione peroxidase activity.

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The whole brain free fatty acid (FFA) level, as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) were determined in the frontal cortex, cerebellum, hippocampus, and pons-medulla region of the single pentylenetetrazol (PZT)-treated and PZT-kindled Hannover-Wistar

Effect of pentylenetetrazol-induced epileptic seizure on the antioxidant enzyme activities, glutathione and lipid peroxidation levels in rat erythrocytes and liver tissues.

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OBJECTIVE In order to clarify whether oxidative stress accompanies epilepsy, we examined the effects of pentylenetetrazol (PTZ)-induced epilepsy on the lipid peroxidation and antioxidant enzyme activities in erythrocytes and liver tissues of adult Wistar rats. METHODS The activities of antioxidative

Anticonvulsant effect of liraglutide, GLP-1 agonist by averting a change in GABA and brain glutathione level on picrotoxin-induced seizures.

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