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succinate dehydrogenase/crise épileptique
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Effectiveness of creatine monohydrate on seizures and oxidative damage induced by methylmalonate.
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Methylmalonic acidemias are metabolic disorders caused by a severe deficiency of methylmalonyl CoA mutase activity, which are characterized by neurological dysfunction, including convulsions. It has been reported that methylmalonic acid (MMA) accumulation inhibits succinate dehydrogenase (SDH) and
Methylmalonate-induced seizures are attenuated in inducible nitric oxide synthase knockout mice.
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Methylmalonic acidemias consist of a group of inherited neurometabolic disorders caused by deficiency of methylmalonyl-CoA mutase activity clinically and biochemically characterized by neurological dysfunction, methylmalonic acid (MMA) accumulation, mitochondrial failure and increased reactive
Intrastriatal methylmalonic acid administration induces rotational behavior and convulsions through glutamatergic mechanisms.
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The effect of intrastriatal administration of methylmalonic acid (MMA), a metabolite that accumulates in methylmalonic aciduria, on behavior of adult male Wistar rats was investigated. After cannula placing, rats received unilateral intrastriatal injections of MMA (buffered to pH 7.4 with NaOH) or
Seizures evoked by mitochondrial toxin, 3-nitropropionic acid: new mechanism of epileptogenesis?
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A number of data concerning the central action of mitochondrial toxins, substances impairing mitochondrial synthesis of ATP and thus compromising cellular energy status, has emerged within last years. 3-Nitropropionic acid (3-NPA) is an irreversible inhibitor of succinate dehydrogenase and
Intrastriatal methylmalonic acid administration induces convulsions and TBARS production, and alters Na+,K+-ATPase activity in the rat striatum and cerebral cortex.
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OBJECTIVE
Methylmalonic acid (MMA) inhibits succinate dehydrogenase (SDH) and beta-hydroxybutyrate dehydrogenase activity in vitro. Acute intrastriatal administration of MMA induces convulsions through glutamatergic mechanisms probably involving primary adenosine triphosphate (ATP) depletion and
Mitochondrial toxin 3-nitropropionic acid evokes seizures in mice.
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3-Nitropropionic acid, a potent inhibitor of succinate dehydrogenase which thus compromises cellular energy metabolism, evoked convulsions in mice in a dose-dependent manner. CD50 for clonic seizures was 158.5 (144.1-174.3) mg/kg. Tonic seizures were not observed. Broad-spectrum anticonvulsants,
Ammonia potentiates methylmalonic acid-induced convulsions and TBARS production.
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Hyperammonemia is a common finding in children with methylmalonic acidemia, an inherited metabolic disease characterized by mental retardation, convulsions, and accumulation of methylmalonic acid (MMA). Although it has been suggested that MMA induces convulsions through succinate dehydrogenase (SDH)
[Succinate oxidation by rat brain mitochondria in experimental convulsions].
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Corasole-induced convulsive fits are accompanied by the activation of succinate oxidation in the isolated mitochondria, paralleled by the mounting effect of factors limiting succinate dehydrogenase activity. Diverse seasonal sensitivity to corasole correlates with the inhibition of
Novel mitochondrial DNA ND5 mutation in a patient with clinical features of MELAS and MERRF.
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BACKGROUND
The mitochondrial DNA gene encoding subunit 5 of complex I (ND5) has turned out to be a hot spot for mutations associated with mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes (MELAS) and various overlap syndromes.
OBJECTIVE
To describe a novel mutation in the
Sporadic paraganglioma caused by de novo SDHB mutations in a 6-year-old girl.
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Germline mutations in the succinate dehydrogenase complex subunit B (SDHB) gene (SDHB) cause susceptibility to paragangliomas and pheochromocytomas; however, it is exceedingly rare in childhood and especially in sporadic cases. We report the first Japanese pediatric case of paraganglioma with a de
Improved method for isolating synaptosomes from 11 regions of one rat brain: electron microscopic and biochemical characterization and use in the study of drug effects on nerve terminal gamma-aminobutyric acid in vivo.
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A procedure is described for the rapid preparation of nerve ending particles (synaptosomes) from 11 regions of one rat brain. The synaptosomal fractions have been characterized by electron microscopy and determination of four marker enzymes, i.e., glutamate decarboxylase (GAD), acetylcholinesterase,
Anticonvulsant and antiproteolytic properties of 2,5-disubstituted oxadiazoles and their inhibition of respiration in rat brain homogenates.
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Eight 2-(3,4-methylenedioxyphenyl)-5-arylamino1,3,4-oxadiazoles were synthesized, characterized by their sharp melting points, elemental analyses, and IR spectra, and evaluated for anticonvulsant activity. The protection afforded by oxadiazoles (100 mg/kg ip) against pentylenetetrazol (90 mg/kg
Creatine protects against the convulsive behavior and lactate production elicited by the intrastriatal injection of methylmalonate.
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Methylmalonic acidemias are metabolic disorders caused by a severe deficiency of methylmalonyl-CoA mutase activity, which are characterized by neurological dysfunction, including convulsions. It has been reported that the accumulating metabolite, L-methylmalonic acid (MMA), inhibits succinate
[Changes in the dehydrogenase and GABA transaminase activity in the cerebral cortex during corazol kindling].
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The experiments on (CBA X C57BL/6)F1 mice have shown that regular corazol injections in subliminal doses stimulated seizure susceptibility (pharmacological kindling). Cytophotometric assay of the activity of oxidative metabolism enzymes (glutamate dehydrogenase, malate dehydrogenase, succinate
The expanding clinical spectrum of mitochondrial diseases.
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The mitochondrion is the only extranuclear organelle containing DNA (mtDNA). As such, genetically determined mitochondrial diseases may result from a molecular defect involving the mitochondrial or the nuclear genome. The first is characterized by maternal inheritance and the second by Mendelian
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