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glutathione reductase/seizures
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m-Trifluoromethyl diphenyl diselenide attenuates glutaric acid-induced seizures and oxidative stress in rat pups: involvement of the γ-aminobutyric acidergic system.
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Glutaric acidemia type I (GA-I) is an inherited metabolic disease characterized by accumulation of glutaric acid (GA) and seizures. The intrastriatal GA administration in rats has been used as an animal model to mimic seizures presented by glutaric acidemic patients. m-Trifluoromethyl diphenyl
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
Effect of inhibition of glutathione reductase by carmustine on central nervous system oxygen toxicity.
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Exposure of animals to O2 at increased partial pressures above 2.5 atmospheres absolute results in seizures. The endogenous intracellular antioxidant defense mechanisms are thought to play a protective role in mitigating such seizures. Investigations were carried out to determine if inhibiting brain
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
Cerebellar oxidative stress and fine motor impairment in adolescent rats exposed to hyperthermia-induced seizures is prevented by maternal caffeine intake during gestation and lactation.
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Febrile seizures (FS) is one of the most common convulsive disorders in infants and young children that only occurs during the first years of life in humans, when the cerebellum is still developing. Several works have shown that maternal caffeine consumption during gestation and lactation can exert
Antioxidant enzymes in cerebral cortex of immature rats following experimentally-induced seizures: upregulation of mitochondrial MnSOD (SOD2).
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We have recently demonstrated the evidence of oxidative stress in brain of immature rats during seizures induced by DL-homocysteic acid (DL-HCA). The aim of the present study was to investigate the antioxidant defense mechanisms under these conditions. Seizures were induced in immature 12-day-old
The Role of NMDA Receptors in the Effect of Purinergic P2X7 Receptor on Spontaneous Seizure Activity in WAG/Rij Rats With Genetic Absence Epilepsy
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P2X7 receptors (P2X7Rs) are ATP sensitive cation channels and have been shown to be effective in various epilepsy models. Absence epilepsy is a type of idiopathic, generalized, non-convulsive epilepsy. Limited data exist on the role of P2X7Rs and no data has been reported regarding the interaction
Seizure-induced changes in mitochondrial redox status.
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The aim of this study was to determine seizure-induced oxidative stress by measuring hippocampal glutathione (GSH) and glutathione disulfide (GSSG) levels in tissue and mitochondria. Kainate-induced status epilepticus (SE) in rats resulted in a time-dependent decrease of GSH/GSSG ratios in both
Valproic acid reduces the intracellular level of glutathione and stimulates human immunodeficiency virus.
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Modifications of the glutathione (GSH) intracellular level have been implicated in the regulation of human immunodeficiency virus (HIV) transcription and expression. In regard to this hypothesis, we have investigated the effects of valproic acid (VPA) on HIV replication. Indeed, it has been recently
The mitochondrial-targeted reactive species scavenger JP4-039 prevents sulfite-induced alterations in antioxidant defenses, energy transfer and cell death signaling in striatum of rats
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Sulfite oxidase (SO) deficiency is a disorder caused either by isolated deficiency of SO or by defects in the synthesis of its molybdenum cofactor. It is characterized biochemically by tissue sulfite accumulation. Patients present with seizures, progressive neurological damage and basal ganglia
Attenuation of cerebral oxygen toxicity by sound conditioning.
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OBJECTIVE
Sound conditioning might reduce cerebral oxygen toxicity.
BACKGROUND
Cerebral oxygen toxicity is related to high levels of reactive oxygen species. Noise-induced hearing loss has been shown to result from ischemia-reperfusion, in which reactive oxygen species play a major role. Repeated
Vitamin U, a novel free radical scavenger, prevents lens injury in rats administered with valproic acid.
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Valproic acid (2-propyl-pentanoic acid, VPA) is the most widely prescribed antiepileptic drug due to its ability to treat a broad spectrum of seizure types. VPA exhibits various side effects such as organ toxicity, teratogenicity, and visual disturbances. S-Methylmethioninesulfonium is a derivative
Brain and liver lipid peroxidation levels following acute and short-term lindane administration in the rat.
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Oxidative stress-related parameters in rat brain and liver were evaluated following acute (60 mg/kg i.p., 2 and 24 h after dosing) or short-term (1000 ppm in the diet for 90 days) lindane administration. Both treatments elicited a significant accumulation of lindane in brain and liver, with
[State of the antioxidant system during induction in rats of primary generalized epileptic activity].
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Antioxidation system in the brain and blood of rats with generalized bemegride-induced epileptic activity was studied. Antioxidation enzyme activity (superoxide dismutase, glutathione peroxidase and glutathione reductase) and alpha-tocopherol content were determined at an early convulsive stage,
In vitro evidence that sulfite impairs glutamatergic neurotransmission and inhibits glutathione metabolism-related enzymes in rat cerebral cortex.
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Sulfite oxidase (SOX) deficiency is an inherited neurometabolic disorder biochemically characterized by tissue accumulation and high urinary excretion of sulfite and thiosulfate. Affected patients present severe neurological dysfunction accompanied by seizures, whose pathophysiology is poorly known.
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