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Pentylenetetrazole-Induced Seizures Are Increased after Kindling, Exhibiting Vitamin-Responsive Correlations to the Post-Seizures Behavior, Amino Acids Metabolism and Key Metabolic Regulators in the Rat Brain.
Int J Mol Sci
August 2023
A.N. Belozersky Institute of Physicochemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia.
Article Synopsis
- Epilepsy is linked to an imbalance between the neurotransmitters glutamate and GABA, leading to increased seizure activities in the brain, which were analyzed using a rat model during pharmacological kindling with PTZ.
- Post-seizure findings showed significant changes, including increased levels of p53 and decreased activity in the 2-oxoglutarate dehydrogenase complex, impacting glutamate degradation and leading to protein acetylation changes.
- The administration of vitamins B1 and B6 influenced these biochemical parameters, modifying correlations between seizure severity and neurotransmitter levels, suggesting potential neuroprotective effects against epilepsy-related seizures.
Vitamin-Responsive Movement Disorders in Children.
Ann Indian Acad Neurol
June 2020
Department of Pediatrics, Lady Hardinge Medical College, New Delhi, India.
Movement disorders in childhood comprise a heterogeneous group of conditions that lead to impairment of voluntary movement, abnormal postures, or inserted involuntary movements. Movement disorders in children are frequently caused by metabolic disorders, both inherited and acquired. Many of these respond to vitamin supplementation.
View Article and Find Full Text PDFMitochondrial complex I mutations in Caenorhabditis elegans produce cytochrome c oxidase deficiency, oxidative stress and vitamin-responsive lactic acidosis.
Hum Mol Genet
February 2004
Canadian Institutes of Health Research Group in Membrane Protein Research, Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.
Mitochondrial dysfunction, with an estimated incidence of 1 in 10 000 live births, is among the most common genetically determined conditions. Missense mutations in the human NDUFV1 gene, which encodes the 51 kDa active site subunit of the NADH-ubiquinone oxidoreductase or complex I, can lead to severe neurological disorders. Owing to the rare and often sporadic nature of mitochondrial disorders, the mechanisms of pathogenesis of most mutations remain poorly understood.
View Article and Find Full Text PDFMitochondrial Disease.
Curr Treat Options Neurol
May 2001
Departments of Neurology and Pediatrics, Columbia University College of Physicians and Surgeons, 710 West 168th Street, New York, NY 10032, USA.
Mitochondrial diseases are disorders of energy metabolism that include defects of pyruvate metabolism, Krebs cycle, respiratory chain (RC), and fatty acid oxidation (FAO). Treatment of pyruvate metabolism, Krebs cycle, and RC disorders is, in general, disappointing. Therapeutic approaches consist of electron acceptors, enzyme activators, vitamins, coenzymes, free-radical scavengers, dietary measures, and supportive therapy.
View Article and Find Full Text PDF[Molecular basis of vitamin-responsive inborn errors of metabolism].
Nihon Rinsho
October 1999
Department of Medical Genetics, Tohoku University School of Medicine.
In inborn errors where the defective enzyme had a cofactor requirement it was found that the administration of large amounts of the vitamin resulted in a clinical and biochemical improvement. A mutation that imposes an exaggerated requirement for a vitamin affects the apoenzyme directly, the conversion of a vitamin into coenzyme, or the attachment of vitamin to the apoenzyme. Direct proof has so far been provided that molecular defects in the said gene underlie both the vitamin-responsive and vitamin-nonresponsive forms.
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