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Pharmacologic rescue of lethal seizures in mice deficient in succinate semialdehyde dehydrogenase.

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Succinate semialdehyde dehydrogenase (ALDH5A1, encoding SSADH deficiency is a defect of 4-aminobutyric acid (GABA) degradation that manifests in humans as 4-hydroxybutyric (gamma-hydroxybutyric, GHB) aciduria. It is characterized by a non-specific neurological disorder including psychomotor

Seizure evolution and amino acid imbalances in murine succinate semialdehyde dehydrogenase (SSADH) deficiency.

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Mice with targeted deletion of the GABA catabolic enzyme succinic semialdehyde dehydrogenase (SSADH) manifest lethal tonic-clonic seizures, amenable to pharmacologic rescue, at 3-4 weeks of life. In the current report, we characterized amino acid profiles in SSADH(-/-) brain utilizing whole brain

[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

[Observations on succinate and lactate dehydrogenase activity following cardiazol convulsions. (A histochemical study with microdensitometrical evaluation)].

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[Effect of the nature of the nutrition and of the functional state of the hypophyseal-adrenal system on the "convulsion readiness" of the body].

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The effect of some amino acids, succinate and different doses of ACTH on the convulsion response readiness of the organism under the action of a strong sound stimulant was studied. With enrichment of the ration with glutamic acid and also following a parenteral introduction of large doses of

Calcium gluconate and sodium succinate for therapy of sodium fluoroacetate experimental intoxication in cats: clinical and electrocardiographic evaluation.

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Sodium fluoroacetate (SFAC) or Compound 1080 is a potent rodenticide, largely used after 1946 for rodent and home pest control. The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and

The effect of diazepam on neonatal seizure: in vivo 31P and 1H NMR study.

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It is assumed that when anticonvulsants arrest seizure, there is rapid return of brain high energy phosphates and brain lactate to control values. To test this hypothesis, diazepam was administered to neonatal dogs during flurothyl-induced seizure. In vivo 31P nuclear magnetic resonance spectroscopy

Mitochondrial encephalomyopathy with decreased succinate-cytochrome c reductase activity.

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We report two siblings with a mitochondrial encephalomyopathy. The syndrome was characterized by ataxia, intellectual impairment, myoclonic jerks, rare seizures, and small stature. Muscle biopsy specimens showed abnormal accumulations of mitochondria and lipid droplets. Biochemical studies on muscle

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

[Clinical and laboratory studies on four Chinese patients with succinate-CoA ligase deficiency noticed by mild methylmalonic aciduria].

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OBJECTIVE To study the clinical and genetic features of the patients with secondary methylmalonic aciduria due to succinate-CoA ligase deficiency. METHODS From February 2011 to April 2014, 4 Chinese patients with succinate-CoA ligase deficiency and mild methylmalonic aciduria were enrolled in this

Five novel SUCLG1 mutations in three Chinese patients with succinate-CoA ligase deficiency noticed by mild methylmalonic aciduria.

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OBJECTIVE Methylmalonic aciduria is the most common organic aciduria in mainland China. Succinate-CoA ligase deficiency causes encephalomyopathy with mitochondrial DNA depletion and mild methylmalonic aciduria. Patients usually present with severe encephalomyopathy, infantile lactic acidosis, which

Murine succinate semialdehyde dehydrogenase (SSADH) deficiency, a heritable disorder of GABA metabolism with epileptic phenotype.

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Murine models of inborn errors of metabolism represent an established approach for investigating pathophysiological mechanisms associated with the corresponding human disorder. Our laboratory studies human inherited defects of GABA synthesis and degradation. One of these, succinate semialdehyde

Liver-directed adenoviral gene transfer in murine succinate semialdehyde dehydrogenase deficiency.

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Murine succinate semialdehyde dehydrogenase (SSADH) deficiency (OMIM 271980; EC 1.2.1.24), a model of the corresponding human disorder, displays 100% mortality at weeks 3-4 of life, associated with lethal tonic-clonic seizures. The biochemical hallmark, gamma-hydroxybutyrate (GHB), accumulates in

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

Succinate increases neuronal post-synaptic excitatory potentials in vitro and induces convulsive behavior through N-methyl-d-aspartate-mediated mechanisms.

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Succinate is a dicarboxylic acid that accumulates due to succinate dehydrogenase inhibition by malonate and methylmalonate exposure. These neurotoxins cause increased excitability and excitotoxic damage, which can be prevented by administering high amounts of succinate. In the present study we

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