Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.9.3.1 (cytochrome oxidase)
8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have determined the complete nucleotide sequence of the circular mitochondrial DNA (mtDNA) of the chytridiomycete fungus, Allomyces macrogynus (57,473 bp; A + T content 60.5%). The identified genes that are typical for most fungal mitochondria include those for the large (rnl) and small subunit (rns) ribosomal RNAs, a complete set of 25 tRNAs, three ATPase subunits (atp6, atp8 and atp9), apocytochrome b(cob), three subunits of the cytochrome oxidase complex (cox1, cox2 and cox3), and seven subunits of the NADH dehydrogenase complex (nad1, nad2, nad3, nad4, nad4L, nad5 and nad6). A total of 28 introns of both groups are found, some of which contain open reading frames (ORFs) coding for potential endonucleases (group I) or reverse-transcriptases (group II). All mitochondrial genes are transcribed from the same DNA strand, as is the case in many other eufungi. Particular features of the A. macrogynus mtDNA include: (1) the first documented case of a fungal mitochondrial ribosomal protein gene (rps3) that is clearly identified by similarity with bacterial homologues; (2) four unique ORFs; (3) the presence of an insert in the atp6 gene that may have been acquired by interspecific transfer; (4) more than 67 short, highly structured and conserved DNA elements inserted in intergenic spacers, introns, and variable regions of the rnl and rns genes: these elements are unusually G + C rich; (5) rRNA structures that resemble more closely those of eubacteria than their counterparts in other fungal mitochondria. The high degree of conservation of the A. macrogynus mitochondrial rRNA secondary structures, the existence of a mitochondrial rps3 gene (common to protist but unique in fungal mtDNAs), and phylogenetic relationships inferred from highly conserved protein genes, demonstrate consistently the ancestral character of this fungal mitochondrial genome.
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PMID:The mitochondrial DNA of Allomyces macrogynus: the complete genomic sequence from an ancestral fungus. 863 71

Heart mitochondria can be made to oxidize extramitochondrial NADH via the exogenous NADH dehydrogenase. Oxidation of extramitochondrial NADH was found to be associated with the disappearance of H+ from the suspension medium. Our studies on the possible pathway through which H+ may disappear from the extramitochondrial space were focused on (i) an unspecific transmembranous H+ leakage along the electrochemical H+ gradient following peroxidative membrane alteration, (ii) stimulation of a controlled H+ reconduction through the H+ channel of the ATP synthase, and (iii) stimulation of the Na+/H+ counterporter by Ca2+ release. Our experiments revealed that none of these H+ pathways was involved in the observed alkalinization of the extramitochondrial space during respiration of external NADH. The latter effect was inhibited when oxidation of external NADH via the respiratory chain was blocked and could be turned into the opposite when artificial e- acceptors of the exogenous NADH dehydrogenase were used to reactivate NADH consumption. Stoichiometric analysis of H+ disappearance and O2 consumption revealed that reducing equivalents of external NADH were transferred to oxygen via cytochrome oxidase and H+ from the suspension was used to release water.
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PMID:The effect of the exogenous NADH dehydrogenase of heart mitochondria on the transmembranous proton movement. 866 Jul 6

The activities of selected enzymes of the respiratory chain system in Onchocerca fasciata (Filarioidea: Onchocercidae) have been investigated histochemically. Thus, the localization and distributions of NADH dehydrogenase (EC 1.6.99.3), succinate dehydrogenase (SDH) (EC 1.3.99.1) and cytochrome oxidase (EC 1.9.3.1) were investigated in various tissues of the adult female worm by employing MTT, Nitro BT (dehydrogenases) and DAB (cytochrome oxidase). Different tissues varied considerably in their enzymatic activities. The hypodermis and reproductive tissues showed strong and identical localization of NADH and SDH dehydrogenase activities reflecting high metabolic rates. Little or no dehydrogenase activities were observed in the intestine and cuticle. In contrast to the two dehyrogenases, no activity was observed for cytochrome oxidase in any of the tissues in adult or embryonic stages of the worm. The significance of these results with respect to the energy metabolism of the worm is discussed. It is suggested that O. fasciata lacks a classical, mammalian-type respiratory pathway and that oxidative phosphorylation is of no importance as an energy generating pathway in this essentially anaerobic parasite.
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PMID:Onchocerca fasciata: histochemical demonstration of succinate and NADH dehydrogenase. 896 Jan 99

The autosomal dominant cerebellar ataxias (ADCA) are a group of neurodegenerative disorders with ataxia and dysarthria as early and dominant signs. In ADCA type II, retinal degeneration causes severe visual impairment. ADCA type II has recently been mapped to chromosome 3p by three independent groups. In the family with ADCA type II studied here, the disease has been mapped to chromosome 3p12-p21.1. Histochemical examination of muscle biopsies in 5 cases showed slight neurogenic atrophy and irregular lobulated appearance or focal decreases of enzyme activity when staining for NADH dehydrogenase, succinic dehydrogenase and cytochrome oxidase. Ragged-red fibres were scarce. Electron microscopic examination showed uneven distribution of mitochondria with large fibre areas devoid of mitochondria and/or large subsarcolemmal accumulations of small rounded mitochondria, and frequent autophagic vacuoles. These vacuoles contained remnants of multiple small rounded organelles, possibly mitochondria, and had a remarkably consistent ultrastructural appearance. Biochemical investigation of mitochondrial function showed reduced activity of complex IV and slightly reduced activity of complex I in the respiratory chain in a severely affected child while no abnormalities were found in his affected uncle.
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PMID:Muscle morphology and mitochondrial investigations of a family with autosomal dominant cerebellar ataxia and retinal degeneration mapped to chromosome 3p12-p21.1. 899 9

The legume Vicia sativa (common vetch) harbors the neurotoxic nonprotein amino acid beta-cyano-L-alanine (BCLA) and its gamma-glutamyl derivative. BCLA elicits hyperexcitability, convulsions, and rigidity in chicks and rats after oral or intraperitoneal administration, but the mechanism of its action is unknown. The effect of different concentrations of BCLA (0.075-10.0 mM) has been investigated in an organotypic tissue culture system. BCLA concentrations of 0.075 and 0.60 mM had no effect, even up to 6 hr. No changes were observed in cultures treated with 1 mM BCLA for 4 hr. BCLA (2.0-10.0 mM) induces concentration-dependent changes in the explants. The explants display neurona vacuolation, chromatin, clumping, and dense shrunken cells, a pathological response generally seen with excitotoxin. MK-801 (35 microM), which blocks the open ion channel associated with the N-methyl-D-aspartate (NMDA) class of glutamate receptors, attenuates the neurotoxic property of BCLA, while the non-NMDA antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (10-20 microM), provides no significant protection. Treatment of isolated mouse brain mitochondria with up to 5 mM BCLA had no inhibitory effect on the activity of NADH dehydrogenase (complex I) or cytochrome or oxidase (complex IV), a cyanide-sensitive enzyme. These results suggest that the neurotoxicity of BCLA (or derivative) is mediated directly or indirectly through NMDA receptors.
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PMID:beta-Cyano-L-alanine toxicity: evidence for the involvement of an excitotoxic mechanism. 902 49

The effect of administration of ethionine on rat liver mitochondrial functions and the protective effect of vitamin E on ethionine induced damage was studied. Ethionine treatment decreased the rate of respiration, respiratory control ratio and P/O ratio. There was a significant decrease in the activities of NADH dehydrogenase, succinate cytochrome C reductase and cytochrome oxidase. A significant decrease was seen on membrane potential and on the levels of ATP. Among the mitochondrial phospholipids only cardiolipin decreased significantly. The lipid peroxide level increased significantly in ethionine treated rats. Administration of vitamin E prior to ethionine treatment relieved the effects (induced by ethionine) on all the parameters studied. This study shows that vitamin E protects against ethionine toxicity.
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PMID:Protective effect of vitamin E against ethionine toxicity. 911 39

The effect of galactosamine on liver mitochondrial functions was studied in vivo in rats at 12hr, 24hr and 36hr after the administration of the drug. State 3 respiration decreased significantly with both NAD+ linked and FAD linked substrates. Respiratory control ratio, an index of membrane integrity and P/O ratio which is a measure of phosphorylation efficiency decreased significantly. There was a significant decrease in the activities of NADH dehydrogenase, succinate dehydrogenase and cytochrome oxidase. A significant decrease was also seen on membrane potential, cytochrome aa3, cytochrome b, cytochrome c and on phospholipids of mitochondria. The observed mitochondrial dysfunctions were related to increased lipid peroxidation, which could cause loss of membrane integrity and a decreased rate of phosphorylation. It is proposed that increased lipid peroxidation was responsible for the inhibition on both oxidation and phosphorylation in mitochondria in galactosamine treated rats.
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PMID:Effect of administration of galactosamine hydrochloride on rat liver mitochondria. 942 49

The complete nucleotide sequence of the Chlamydomonas eugametos (Chlamydomonadales, Chlorophyceae, sensu Mattox and Stewart) mitochondrial genome has been determined (22,897 bp, 34.6% G + C). The genes identified in this circular-mapping genome include those for apocytochrome b, subunit 1 of the cytochrome oxidase complex, subunits 1, 2, 4, 5, and 6 of the NADH dehydrogenase complex, discontinuous large and small subunit ribosomal rRNAs and three tRNAs whose anticodons CAU, CCA and UUG are specific for methionine, tryptophan and glutamine, respectively. The C. eugametos mitochondrial DNA (mtDNA), therefore, shares almost the same reduced set of coding functions and similar unusual features of rRNA gene organization with the linear 15.8 kb mtDNA of Chlamydomonas reinhardtii, the only other completely sequenced chlamydomonadalean mtDNA. However, sequence analysis of the C. eugametos mtDNA has revealed the following distinguishing features relative to those of C. reinhardtii: (1) the absence of a reverse transcriptase-like gene homologue, (2) the presence of an additional gene for tRNA(met) that may be a pseudogene, (3) a completely different gene order, (4) transcription of all genes from the same mtDNA strand, (5) a lower G + C content, (6) less pronounced bias in codon usage, and (7) nine group I introns, several of which contain open reading frames coding for potential maturases/endonucleases and two have a nucleotide at the 5' or 3' splice site of the deduced precursor RNAs that deviates from highly conserved nucleotides reported in other group I introns. The features of mitochondrial genome organization and gene content shared by C. eugametos and C. reinhardtii contrast with those of other green algal mtDNAs that have been characterized in detail. The deep evolutionary divergence between these two Chlamydomonas taxa within the Chlamydomonadales suggests that their shared features of mitochondrial genome organization evolved prior to the origin of this group.
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PMID:Complete sequence of the mitochondrial DNA of Chlamydomonas eugametos. 948 40

The organization of the mitochondrial maxicircle genome of Trypanosoma brucei is unique in the close packing of the mRNA genes. For many of them, the 5' and 3' ends of adjacent transcripts overlap and formation of the proper 3' or 5' end can eliminate a portion of the coding sequence of the adjacent gene. Large, polycistronic transcripts have been detected. suggesting that mechanisms for precise cleavages at both 5' and 3' gene boundaries must exist. However, no common sequences near the ends of the mRNAs that could be candidates for control regions have been detected. In addition, nothing is known about how RNA editing interacts with and affects 5' and 3' processing and/or polyadenylation. Edited precursor transcripts have been detected, indicating that editing complexes can assemble prior to transcript cleavage. Because editing often initiates near the 3' end of the mRNA, the assembly of an editing complex in this region may influence the cleavage selection process. In order to determine the extent that RNA editing and 3' end-processing interact, RNAs were analyzed to determine the extent of editing in precursor RNAs and to determine if unedited transcripts can be cleaved and polyadenylated. Two overlapping RNA junctions were analyzed; the junction between NADH dehydrogenase (ND) subunit 7 and cytochrome oxidase (CO) subunit III, and the junction between CO subunit II and maxicircle unidentified reading frame (MURF) II. For both of these RNAs, editing affects restriction endonuclease recognition sequences, allowing us to analyze editing patterns by differential restriction digests. These analyses suggest that when the gRNA is supplied in trans, RNA editing and cleavage/polyadenylation are independent events and while they may influence one another, one event is not dependent on the other. Conversely, for the COII transcript, where the gRNA is located at the 3' end of the mRNA and appears to be supplied in cis, edited precursors were not detected. This suggests a requirement for a precise intramolecular interaction for COII editing that cannot form prior to 3' end-maturation.
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PMID:Mitochondrial mRNA 3' cleavage/polyadenylation and RNA editing in Trypanosoma brucei are independent events. 949 34

The effect of alpha-tocopherol pretreatment (6 mg/100 g body wt/day, orally for a period of 90 days) on mitochondrial electron transport in myocardial infarction induced by isoproterenol (20 mg/100 g body wt, subcutaneously for two days) was studied in rats. A significant decrease was observed in the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase and cytochrome oxidase in heart mitochondria of isoproterenol administered rats. The cytochrome content and the oxidation of succinate in state 3 and state 4 decreased significantly in the cardiac mitochondria treatment. In alpha-tocopherol pretreated rats, the activities of TCA cycle enzymes, concentration of cytochromes and the oxidation of succinate in state 3 and state 4 were retained at near normal values, following isoproterenol administration.
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PMID:Effect of alpha-tocopherol on mitochondrial electron transport in experimental myocardial infarction in rats. 975 71


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