Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.5 (NADH dehydrogenase)
 2,135 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper, we present the nucleotide sequence of a 5248 bp-long region of the mitochondrial (mt) genome of the dermatophyte Trichophyton rubrum. This region which represents about 1/4 of the total mt genome of this species reveals a compact organization of genes including: the glutaminyl tRNA, the methionyl tRNA, the cytochrome oxidase subunit I gene, the arginyl tRNA, the mitochondrial version of the ATPase subunit 9 gene, the cytochrome oxidase subunit II gene and a part of the NADH dehydrogenase ND4L and ND5 gene "complex". The main features of the part of mt DNA sequenced is the non-interrupted COXI gene and the presence in the mitochondrial version of the ATPase 9 gene of a small group IA intron. The extensive amino-acid sequence similarity with the equivalent gene in Aspergillus nidulans and Neuropora crassa indicates that this gene codes for a dicyclohexylcarbodiimide binding protein. The conserved arrangement of this portion of the mt genome and the presence of tRNAs between the protein-coding genes are compatible with a large polycistronic transcript processed by the excision of tRNAs, or similar secondary structures, as proposed for other fungal or mammalian mt DNAS.
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PMID:Mitochondrial DNA sequence analysis of the cytochrome oxidase subunit I and II genes, the ATPase9 gene, the NADH dehydrogenase ND4L and ND5 gene complex, and the glutaminyl, methionyl and arginyl tRNA genes from Trichophyton rubrum. 132 16

3,4-Methylenedioximethamphetamine (MDMA, ecstasy) is a worldwide abused stimulant drug, with persistent neurotoxic effects and high prevalence among adolescents. The massive release of 5-HT from pre-synaptic storage vesicles induced by MDMA followed by monoamine oxidase B (MAO-B) metabolism, significantly increases oxidative stress at the mitochondrial level. l-Carnitine and its ester, acetyl-l-carnitine (ALC), facilitate the transport of long chain free fatty acids across the mitochondrial membrane enhancing neuronal anti-oxidative defense. Here, we show the potential of ALC against the neurotoxic effects of MDMA exposure. Adolescent male Wistar rats were assigned to four groups: control saline solution, isovolumetric to the MDMA solution, administered i.p.; MDMA (4x10 mg/kg MDMA, i.p.); ALC/MDMA (100 mg/kg 30 min of ALC prior to MDMA, i.p.) and ALC (100 mg/kg, i.p.). Rats were killed 2 weeks after exposure and brains were analyzed for lipid peroxidation, carbonyl formation, mitochondrial DNA (mtDNA) deletion and altered expression of the DNA-encoded subunits of the mitochondrial complexes I (NADH dehydrogenase, NDII) and IV (cytochrome c oxidase, COXI) from the respiratory chain. Levels of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) were also assessed. The present work is the first to successfully demonstrate that pretreatment with ALC exerts effective neuroprotection against the MDMA-induced neurotoxicity at the mitochondrial level, reducing carbonyl formation, decreasing mtDNA deletion, improving the expression of the respiratory chain components and preventing the decrease of 5-HT levels in several regions of the rat brain. These results indicate potential benefits of ALC application in the prevention and treatment of neurodegenerative disorders.
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PMID:Acetyl-L-carnitine provides effective in vivo neuroprotection over 3,4-methylenedioximethamphetamine-induced mitochondrial neurotoxicity in the adolescent rat brain. 1901 3