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ubiquinone/seizures
Veza se sprema u međuspremnik
Stranica 1 iz 19 rezultatima
Neuropharmacological effects of lipoic acid and ubiquinone on δ-aminolevulinic dehydratase, Na(+) , K(+) -ATPase, and Mg(2+) -ATPase activities in rat hippocampus after pilocarpine-induced seizures.
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In this study, we investigated the effects of lipoic acid (LA) in the hippocampus oxidative stress caused by pilocarpine-induced seizures in adult rats. Wistar rats were treated with 0.9% saline (i.p., control group), LA (10mg/kg, i.p., LA group), ubiquinone [20mg/kg, i.p., ubiquinone (UQ) group],
Neuropharmacological effects of lipoic acid and ubiquinone on the mRNA level of interleukin-1β and acetylcholinesterase activity in rat hippocampus after seizures.
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The purpose of this study was to investigate the neuroprotective effects of lipoic acid and ubiquinone on interleukin-1β (IL-1β) mRNA levels and acetylcholinesterase (AChE) activities in rat hippocampus after pilocarpine-induced seizures. Wistar rats were intraperitoneally administered with either
Effects of ubiquinone on hydroperoxide concentration and antioxidant enzymatic activities in the rat hippocampus during pilocarpine-induced seizures.
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Recent researches have shown that antioxidant compounds may have certain neuroprotective effect against the neurotoxicity of seizures at cellular level. Ubiquinone (UQ), an antioxidant compound, exhibits a wide range of therapeutic effects that are attributed to its potent antioxidant capacity. The
CABC1 gene mutations cause ubiquinone deficiency with cerebellar ataxia and seizures.
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Coenzyme Q(10) (CoQ(10)) plays a pivotal role in oxidative phosphorylation (OXPHOS) in that it distributes electrons between the various dehydrogenases and the cytochrome segments of the respiratory chain. Primary coenzyme Q(10) deficiency represents a clinically heterogeneous condition suggestive
The calculation of the mitochondrial free [NAD+]/[NADH][H+] ratio in brain: effect of electroconvulsive seizure.
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This study is an investigation into the validity of calculating the mitochondrial redox state in brain in vivo using models of seizure and anoxia in rats. At six intervals following electroconvulsive seizure (0.5-10 min) and after 5 min of complete anoxia, multiple metabolites were measured in
Pathogenic mutations of the human mitochondrial citrate carrier SLC25A1 lead to impaired citrate export required for lipid, dolichol, ubiquinone and sterol synthesis.
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Missense mutations of the human mitochondrial citrate carrier, encoded by the SLC25A1 gene, lead to an autosomal recessive neurometabolic disorder characterised by neonatal-onset encephalopathy with severe muscular weakness, intractable seizures, respiratory distress, and lack of psychomotor
Neuroprotective effects of idebenone against pilocarpine-induced seizures: modulation of antioxidant status, DNA damage and Na(+), K (+)-ATPase activity in rat hippocampus.
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The current study investigated the neuroprotective activity of idebenone against pilocarpine-induced seizures and hippocampal injury in rats. Idebenone is a ubiquinone analog with antioxidant, and ATP replenishment effects. It is well tolerated and has low toxicity. Previous studies reported the
Abnormal carbohydrate metabolism in cerebrospinal fluid in Rett syndrome.
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We analyzed lactate, pyruvate, and citric acid cycle intermediates in cerebrospinal fluid by high-performance liquid chromatography in Rett syndrome patients (n = 27; mean age, 5.7 +/- 3.4 years) and age-matched female controls (n = 12; mean age, 7.0 +/- 3.3 years). The lactate, pyruvate,
Whole Exome Sequencing Identifies the Genetic Basis of Late-Onset Leigh Syndrome in a Patient with MRI but Little Biochemical Evidence of a Mitochondrial Disorder.
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Leigh syndrome is a subacute necrotising encephalomyopathy proven by post-mortem analysis of brain tissue showing spongiform lesions with vacuolation of the neuropil followed by demyelination, gliosis and capillary proliferation caused by mutations in one of over 75 different genes, including
Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes with special reference to the mechanism of cerebral manifestations.
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A 29-year-old man with mitochondrial encephalomyopathy caused by partial deficiency of mitochondrial NADH-ubiquinone oxidoreductase (Complex I) is described. Clinical manifestations were characterized by generalized convulsion, dementia and stroke-like episodes consisting of hemianopsia, Gerstmann's
Auditory symptoms: a critical clue for diagnosis of MELAS.
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Mitochondrial encephalopathy, lactic acidosis with stroke-like episodes (MELAS) is a rare mitochondrial disorder that affects adults. MELAS syndrome can mimic cerebrovascular disease, encephalitis or toxic-metabolic encephalopathy. The authors reported two patients who presented with auditory
Hypothalamic digoxin-mediated model for epileptogenesis.
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OBJECTIVE
This study assessed the changes in the isoprenoid pathway and its metabolites in seizure disorder (ILAE classification - I generalized - idiopathic generalized epilepsy with age-related onset - epilepsy with generalized tonic clonic seizures on awakening) and the metabolic cascade produced
Mitochondrial complex I encephalomyopathy and cerebral 5-methyltetrahydrofolate deficiency.
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Folate transport to the brain depends on ATP-driven folate receptor-mediated transport across choroid plexus epithelial cells. Failure of ATP production in Kearns-Sayre syndrome syndrome provides one explanation for the finding of low spinal fluid (CSF) 5-methyltetrahydrofolate (5MTHF) levels in
Novel recessive mutations in COQ4 cause severe infantile cardiomyopathy and encephalopathy associated with CoQ10 deficiency.
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Coenzyme Q10 (CoQ10) or ubiquinone is one of the two electron carriers in the mitochondrial respiratory chain which has an essential role in the process of oxidative phosphorylation. Defects in CoQ10 synthesis are usually associated with the impaired function of CoQ10-dependent complexes I, II and
Mutations in COQ4, an essential component of coenzyme Q biosynthesis, cause lethal neonatal mitochondrial encephalomyopathy.
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BACKGROUND
The identification of the molecular basis of mitochondrial disorders continues to be challenging and expensive. The increasing usage of next-generation sequencing is facilitating the discovery of the genetic aetiology of heterogeneous phenotypes associated with these conditions. Coenzyme
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