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[PMID]:26319306
[Au] Autor:Vasquez NP; Crosnier de Bellaistre-Bonose M; Lévêque N; Thioulouse E; Doummar D; Billette de Villemeur T; Rodriguez D; Couderc R; Robin S; Courderot-Masuyer C; Moussa F
[Ad] Endereço:Univ Paris-Sud, LETIAM, Lip(Sys)(2), IUT d'Orsay, Plateau de Moulon, 91400 Orsay, France; SARL BIOEXIGENCE, Espace Lafayette, rue Alfred de Vigny 8, 25000 Besançon, France.
[Ti] Título:Advances in the metabolic profiling of acidic compounds in children's urines achieved by comprehensive two-dimensional gas chromatography.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1002:130-8, 2015 Oct 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The main objective of this work was to evaluate a comprehensive two-dimensional gas chromatographic (GCxGC) coupled to quadrupole mass spectrometry (qMS) method in the field of biomarker candidates' discovery. To this purpose we developed a GCxGC-qMS method suitable for the separation of organic acids and other classes of compounds with silylable polar hydrogen such as sugars, amino-acids, and vitamins. As compared to those obtained by a widely used 1D-GC method, the urinary chromatographic profiles performed by the proposed 2D-GC method exhibit higher resolution and sensitivity, leading to the detection of up to 92 additional compounds in some urine samples including some well-known biomarkers. In order to validate the proposed method we focused on three metabolites of interest with various functional groups and polarities including CH3-malonic acid (MMA: biomarker of methylmalonic acidemia), 3-hydroxy-3-methyl-glutaric acid (3-OHMGA: biomarker of 3-hydroxy-3-methylglutaric acidemia), and phenylpiruvic acid (PhPA: marker of phenylketonuria). While these three metabolites can be considered as representative of organic acids classically determined by 1D-GC, they cannot be representative of new detected metabolites. Thus, we also focused on quinolic acid (QUIN), taken as an example of biomarker not detected at basal levels with the classical 1D GC-qMS method. In order to obtain sufficient recoveries for all tested compounds, we developed a sample preparation protocol including a step of urea removal followed by two extraction steps using two solvents of different polarity and selectivity. Recoveries with the proposed method reached more than 80% for all targeted compounds and the linearity was satisfactory up to 50µmol/L. The CVs of the within-run and within-laboratory precisions were less than 8% for all tested compounds. The limits of quantification (LOQs) were 0.6µmol/L for MMA, 0.4µmol/L for 3-OHMGA, 0.7µmol/L for PhPA, and 1µmol/L for QUIN. The LOQs of these metabolites obtained by a classical GC-MS method under the same chromatographic conditions were 5µmol/L for MMA, 4µmol/L for 3-OHMGA, 6µmol/L for PhPA while QUIN was below the limit of detection. As compared to 1D-GC, these results highlight the enhanced detectability of urine metabolites by the 2D-GC technique. Our results also show that for each new detected compound it is necessary to develop and validate an appropriate sample preparation procedure.
[Mh] Termos MeSH primário: Cromatografia Gasosa/métodos
Cromatografia Gasosa-Espectrometria de Massas/métodos
Ácidos Quinolínicos/urina
[Mh] Termos MeSH secundário: Criança
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Quinolinic Acids)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150924
[Lr] Data última revisão:
150924
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150831
[St] Status:MEDLINE


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[PMID]:25496808
[Au] Autor:Kikuchi H; Suzuki T; Ogura M; Homma MK; Homma Y; Oshima Y
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba-yama, Aoba-ku, Sendai 980-8578, Japan. Electronic address: hal@mail.pharm.tohoku.ac.jp.
[Ti] Título:Synthesis of prenylated quinolinecarboxylic acid derivatives and their anti-obesity activities.
[So] Source:Bioorg Med Chem;23(1):66-72, 2015 Jan 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondrial uncoupling is one of the therapeutic strategies used to control energy metabolism in various metabolic diseases and in obesity. Ppc-1 (1), a prenylated quinolinecarboxylic acid isolated from cellular slime molds, shows uncoupling activity in vitro and anti-obesity activity in vivo. In this study, we synthesized Ppc-1 (1) and its derivatives, and revealed the structure-activity relationship of uncoupling activities. The triprenylated compound 18 showed mitochondrial uncoupling activity that was more potent than that of Ppc-1 (1). Compound 18 also suppressed weight gain in mice without undesired effects such as lesions on tissues. These results indicate that compound 18 could be used as a seed compound for new anti-obesity drugs.
[Mh] Termos MeSH primário: Fármacos Antiobesidade/síntese química
Fármacos Antiobesidade/farmacologia
Obesidade/tratamento farmacológico
Ácidos Quinolínicos/síntese química
Ácidos Quinolínicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Fármacos Antiobesidade/química
Camundongos
Camundongos Endogâmicos ICR
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Obesidade/metabolismo
Prenilação
Ácidos Quinolínicos/química
Relação Estrutura-Atividade
Desacopladores/síntese química
Desacopladores/química
Desacopladores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Quinolinic Acids); 0 (Uncoupling Agents)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:141222
[Lr] Data última revisão:
141222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141216
[St] Status:MEDLINE


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[PMID]:22392362
[Au] Autor:Kalonia H; Mishra J; Kumar A
[Ad] Endereço:Pharmacology Division, UGC Centre of Advanced Study, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.
[Ti] Título:Targeting neuro-inflammatory cytokines and oxidative stress by minocycline attenuates quinolinic-acid-induced Huntington's disease-like symptoms in rats.
[So] Source:Neurotox Res;22(4):310-20, 2012 Nov.
[Is] ISSN:1476-3524
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent experimental and clinical reports support the fact that the minocycline exhibits significant neuroprotective activity in neurodegenerative diseases. However, its mechanism of neuroprotection is still far from our understanding. Besides, minocycline does not always produce neuroprotective effect. Therefore, this study has been designed to explore the possible mechanism of minocycline in experimental model of HD in rats. Intrastriatal administration of quinolinic acid caused a significant reduction in body weight, motor dysfunction (impaired locomotor activity, rotarod performance, and beam walk test), oxidative damage (as evidenced by increase in lipid peroxidation, nitrite concentration, and depletion of super oxide dismutase and catalase), increased TNF-α and IL-6 levels as compared to the sham-treated animals. Minocycline (25, 50, and 100 mg/kg) treatment (for 21 days) significantly improved body weight, locomotor activity, rotarod performance, balance beam walk performance, oxidative defense, attenuated TNF-α and IL-6 levels as compared to quinolinic-acid (QA)-treated animals. This study provides evidence that minocycline might have neuroprotective effect against QA-induced Huntington-like behavioral, biochemical alterations, and neuroinflammation in rats.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Doença de Huntington
Minociclina/uso terapêutico
Estresse Oxidativo/efeitos dos fármacos
Ácidos Quinolínicos/toxicidade
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Peso Corporal/efeitos dos fármacos
Catalase/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Esquema de Medicação
Doença de Huntington/induzido quimicamente
Doença de Huntington/tratamento farmacológico
Doença de Huntington/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Atividade Motora/efeitos dos fármacos
Nitritos/metabolismo
Desempenho Psicomotor/efeitos dos fármacos
Ratos
Ratos Wistar
Teste de Desempenho do Rota-Rod
Estatística como Assunto
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Nitrites); 0 (Quinolinic Acids); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); FYY3R43WGO (Minocycline)
[Em] Mês de entrada:1302
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120307
[St] Status:MEDLINE


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[PMID]:21830834
[Au] Autor:Tallec G; Fries PH; Imbert D; Mazzanti M
[Ad] Endereço:Laboratoire de Reconnaissance Ionique et Chimie de Coordination, SCIB, UMR-E 3 CEA/UJF-Grenoble 1, INAC, Grenoble, F-38054, France.
[Ti] Título:High relaxivity and stability of a hydroxyquinolinate-based tripodal monoaquagadolinium complex for use as a bimodal MRI/optical imaging agent.
[So] Source:Inorg Chem;50(17):7943-5, 2011 Sep 05.
[Is] ISSN:1520-510X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An octadentate ligand based on triazacyclononane and 8-hydroxyquinolinate/phenolate binding units leads to very soluble, highly stable lanthanide complexes. The monoaquagadolinium complex shows a high relaxivity as a result of the unusually long rotational correlation time, fast water exchange rate, and slow electronic relaxation. The ligand also acts as sensitizer of the near-IR luminescence emission of the Yb and Nd ions. It appears as an excellent candidate for use as a bimodal imaging agent.
[Mh] Termos MeSH primário: Meios de Contraste/química
Gadolínio/química
Imagem por Ressonância Magnética
Compostos Organometálicos/química
Ácidos Quinolínicos/química
[Mh] Termos MeSH secundário: Meios de Contraste/síntese química
Hidroxibenzoatos/química
Ligantes
Luminescência
Estrutura Molecular
Neodímio/análise
Compostos Organometálicos/síntese química
Espectroscopia de Luz Próxima ao Infravermelho
Itérbio/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Contrast Media); 0 (Hydroxybenzoates); 0 (Ligands); 0 (Organometallic Compounds); 0 (Quinolinic Acids); 29656-58-4 (phenolic acid); 2I87U3734A (Neodymium); AU0V1LM3JT (Gadolinium); MNQ4O4WSI1 (Ytterbium)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110812
[St] Status:MEDLINE
[do] DOI:10.1021/ic2012793


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[PMID]:21146500
[Au] Autor:Mozrzymas J; Szczesny T; Rakus D
[Ad] Endereço:Department of Animal Molecular Physiology and Laboratory of Cellular Neurobiology, Institute of Zoology, Wroclaw University, Cybulskiego 30, 50-205 Wroclaw, Poland.
[Ti] Título:The effect of glycogen phosphorolysis on basal glutaminergic transmission.
[So] Source:Biochem Biophys Res Commun;404(2):652-5, 2011 Jan 14.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Astrocytic glycogen metabolism sustains neuronal activity but its impact on basal glutamatergic synaptic transmission is not clear. To address this issue, we have compared the effect of glycogen breakdown inhibition on miniature excitatory postsynaptic currents (mEPSCs) in rat hippocampal pure neuronal culture (PNC) and in astrocyte-neuronal co-cultures (ANCC). Amplitudes of mEPSC in ANCC were nearly twice as large as in PNC with no difference in current kinetics. Inhibition of glycogen phosphorylase reduced mEPSC amplitude by roughly 40% in ANCC being ineffective in PNC. Altogether, these data indicate that astrocyte-neuronal interaction enhances basal mEPSCs in ANCC mainly due to astrocytic glycogen metabolism.
[Mh] Termos MeSH primário: Ácido Glutâmico/metabolismo
Glicogênio/metabolismo
Hipocampo/fisiologia
Transmissão Sináptica
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Astrócitos/fisiologia
Técnicas de Cocultura
Glicogênio Fosforilase/antagonistas & inibidores
Glicogênio Fosforilase/metabolismo
Hipocampo/citologia
Hipocampo/metabolismo
Neurônios/metabolismo
Neurônios/fisiologia
Ácidos Quinolínicos/farmacologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bay W1807); 0 (Quinolinic Acids); 3KX376GY7L (Glutamic Acid); 9005-79-2 (Glycogen); EC 2.4.1.- (Glycogen Phosphorylase)
[Em] Mês de entrada:1102
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:101215
[St] Status:MEDLINE
[do] DOI:10.1016/j.bbrc.2010.12.033


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[PMID]:18243165
[Au] Autor:Velloso NA; Dalmolin GD; Fonini G; Gindri Sinhorin VD; Ferreira da Silveira A; Rubin MA; Mello CF
[Ad] Endereço:Department of Chemistry, Center of Exact and Natural Sciences, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil.
[Ti] Título:Spermine attenuates behavioral and biochemical alterations induced by quinolinic acid in the striatum of rats.
[So] Source:Brain Res;1198:107-14, 2008 Mar 10.
[Is] ISSN:0006-8993
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Polyamines are aliphatic amines containing nucleophilic centers that are found in all eukaryotic cells, including brain cells. These compounds determine neuroprotection in experimental models of cerebral ischemia and neurotoxicity. In the current study we investigated the protective effects of spermine, an agonist of the polyamine binding site at the N-methyl-d-aspartate receptor, against the behavioral and neurochemical alterations induced by quinolinic acid. The unilateral intrastriatal injection of quinolinic acid (180 nmol/site into the dorsal striatum) induced stereotypical motor asymmetries, assessed by the open field and elevated body swing tests. Spermine modulated quinolinic acid-induced rotational behavior biphasically. While the previous intrastriatal administration of spermine at the dose of 0.1 nmol/site increased, the administration of spermine at the dose of 10 nmol/site reduced quinolinic acid-induced rotational behavior. Spermine (10 nmol/site) also decreased the contralateral swing behavior induced by quinolinic acid. Furthermore, the effect of 10 nmol of spermine was counteracted by the co-administration of arcaine (10 nmol), a selective antagonist of the polyamine binding site at the N-methyl-d-aspartate receptor. In addition, spermine (10 nmol) protected against quinolinic acid-induced protein carbonylation in the rat striatum, further suggesting an antioxidant role for this polyamine. These results provide evidence that the behavioral and biochemical alterations induced by quinolinic acid are attenuated or prevented by spermine through its interaction with N-methyl-d-aspartate receptor and/or its antioxidant function.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Química Encefálica/fisiologia
Corpo Estriado/metabolismo
Estresse Oxidativo/fisiologia
Receptores de N-Metil-D-Aspartato/metabolismo
Espermina/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Comportamento Animal/efeitos dos fármacos
Comportamento Animal/fisiologia
Biguanidas/farmacologia
Sítios de Ligação/efeitos dos fármacos
Sítios de Ligação/fisiologia
Ligação Competitiva/efeitos dos fármacos
Ligação Competitiva/fisiologia
Química Encefálica/efeitos dos fármacos
Corpo Estriado/efeitos dos fármacos
Relação Dose-Resposta a Droga
Antagonistas de Aminoácidos Excitatórios/farmacologia
Masculino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Estresse Oxidativo/efeitos dos fármacos
Ácidos Quinolínicos/antagonistas & inibidores
Ácidos Quinolínicos/farmacologia
Ratos
Ratos Wistar
Receptores de N-Metil-D-Aspartato/efeitos dos fármacos
Espermina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biguanides); 0 (Excitatory Amino Acid Antagonists); 0 (Quinolinic Acids); 0 (Receptors, N-Methyl-D-Aspartate); 2FZ7Y3VOQX (Spermine); 544-05-8 (arcaine)
[Em] Mês de entrada:0806
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080205
[St] Status:MEDLINE
[do] DOI:10.1016/j.brainres.2007.12.056


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[PMID]:17962329
[Au] Autor:Wrighton DC; Baker EJ; Chen PE; Wyllie DJ
[Ad] Endereço:Centre for Neuroscience Research, Hugh Robson Building, University of Edinburgh, George Square, Edinburgh, UK.
[Ti] Título:Mg2+ and memantine block of rat recombinant NMDA receptors containing chimeric NR2A/2D subunits expressed in Xenopus laevis oocytes.
[So] Source:J Physiol;586(1):211-25, 2008 Jan 01.
[Is] ISSN:0022-3751
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:N-methyl-d-aspartate receptors (NMDARs) display differences in their sensitivity to the channel blockers Mg(2+) and memantine that are dependent on the identity of the NR2 subunit present in the receptor-channel complex. This study used two-electrode voltage-clamp recordings from Xenopus laevis oocytes expressing recombinant NMDARs to investigate the actions of Mg(2+) and memantine at the two NMDARs displaying the largest differences in sensitivity to these blockers, namely NR1/NR2A and NR1/NR2D NMDARs. In addition, NR2A/2D chimeric subunits have been employed to examine the effects of pore-forming elements and ligand-binding domains (LBD) on the potency of the block produced by each of these inhibitors. Our results show that, as previously documented, NR2D-containing NMDARs are less sensitive to voltage-dependent Mg(2+) block than their NR2A-containing counterparts. The reduced sensitivity is determined by the M1M2M3 membrane-associated regions, as replacing these regions in NR2A subunits with those found in NR2D subunits results in a approximately 10-fold reduction in Mg(2+) potency. Intriguingly, replacing the NR2A LBD with that from NR2D subunits results in a approximately 2-fold increase in Mg(2+) potency. Moreover, when responses mediated by NR1/NR2A NMDARs are evoked by the partial agonist homoquinolinate, rather than glutamate, Mg(2+) also displays an increased potency. Memantine block of glutamate-evoked currents is most potent at NR1/NR2D NMDARs, but no differences are observed in its ability to inhibit NR2A-containing or NR2A/2D chimeric NMDARs. We suggest that the potency of block of NMDARs by Mg(2+) is influenced not only by pore-forming regions but also the LBD and the resulting conformational changes that occur following agonist binding.
[Mh] Termos MeSH primário: Dopaminérgicos/farmacologia
Magnésio/farmacologia
Memantina/farmacologia
Oócitos/metabolismo
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Quimera
Relação Dose-Resposta a Droga
Eletrofisiologia
Potenciais Evocados/efeitos dos fármacos
Feminino
Ácido Glutâmico/farmacologia
Oócitos/efeitos dos fármacos
Técnicas de Patch-Clamp
Ácidos Quinolínicos/farmacologia
Ratos
Receptores de N-Metil-D-Aspartato/efeitos dos fármacos
Receptores de N-Metil-D-Aspartato/metabolismo
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dopamine Agents); 0 (NR2A NMDA receptor); 0 (NR2D NMDA receptor); 0 (Quinolinic Acids); 0 (Receptors, N-Methyl-D-Aspartate); 3KX376GY7L (Glutamic Acid); 490-75-5 (homoquinolinic acid); I38ZP9992A (Magnesium); W8O17SJF3T (Memantine)
[Em] Mês de entrada:0805
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:071027
[St] Status:MEDLINE


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[PMID]:17693424
[Au] Autor:Gregus Z; Németi B
[Ad] Endereço:Department of Pharmacology and Pharmacotherapy, Toxicology Section, University of Pécs, Medical School, Szigeti út 12, H-7624 Pécs, Hungary. zoltan.gregus@aok.pte.hu
[Ti] Título:Glutathione-dependent reduction of arsenate by glycogen phosphorylase responsiveness to endogenous and xenobiotic inhibitors.
[So] Source:Toxicol Sci;100(1):44-53, 2007 Nov.
[Is] ISSN:1096-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rabbit muscle glycogen phosphorylase-a (GPa) reduces arsenate (As(V)) to the more toxic arsenite (As(III)) in a glutathione (GSH)-dependent fashion. To determine whether reduction of As(V) by GPa is countered by compounds known to inhibit GP-catalyzed glycogenolysis, the effects of thiol reagents, endogenous compounds (glucose, ATP, ADP) as well as nonspecific glycogen phosphorylase inhibitors (GPIs; caffeine, quercetin, flavopiridol [FP]), and specific GPIs (1,4-dideoxy-1,4-imino-D-arabinitol [DAB], BAY U6751, CP320626) were tested on reduction of As(V) by rabbit muscle GPa in the presence of glycogen (substrate), AMP (activator), and GSH, and the As(III) formed from As(V) was quantified by high-performance liquid chromatography-hydride generation-atomic fluorescence spectrometry. The As(V)-reducing activity of GPa was moderately sensitive to thiol reagents. Glucose above 5mM and ADP or ATP at physiological levels diminished GPa-catalyzed As(V) reduction. All GPIs inhibited As(V) reduction by GPa in a concentration-dependent fashion; however, their effects were differentially affected by glucose (10mM) or AMP (200microM instead of 25microM), known modulators of the action of some GPIs on the GP-catalyzed glycogenolysis. Inhibition of As(V) reduction by DAB and quercetin was not influenced by glucose or AMP. Glucose that potentiates the inhibitory effects of caffeine, BAY U6751, and CP320626 on the glycogenolytic activity of GPa also enhanced the inhibitory effects of these GPIs on GPa-catalyzed As(V) reduction. AMP at high concentration alleviated the inhibition by BAY U6751 and CP320626 (whose antagonistic effect on GP-catalyzed glycogen breakdown is also AMP sensitive), whereas the inhibition in As(V) reduction by FP or caffeine was little affected by AMP. Thus, GPIs inhibit both the glycogenolytic and As(V)-reducing activities of GP, supporting that the latter is coupled to glycogenolysis. It was also shown that a GPa-rich extract of rat liver contained GSH-dependent As(V)-reducing activity that was inhibited by specific GPIs, suggesting that the liver-type GPa can also catalyze reduction of As(V).
[Mh] Termos MeSH primário: Arseniatos/metabolismo
Arsenitos/metabolismo
Inibidores Enzimáticos/farmacologia
Glutationa/metabolismo
Glicogênio Fosforilase Hepática/antagonistas & inibidores
Glicogênio Fosforilase Muscular/antagonistas & inibidores
Glicogenólise/efeitos dos fármacos
Xenobióticos/farmacologia
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Monofosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Amidas/farmacologia
Animais
Arabinose/farmacologia
Cafeína/farmacologia
Cromatografia Líquida de Alta Pressão
Relação Dose-Resposta a Droga
Glucose/metabolismo
Glucose-6-Fosfato/metabolismo
Glicogênio/metabolismo
Glicogênio Fosforilase Hepática/metabolismo
Glicogênio Fosforilase Muscular/metabolismo
Imino Furanoses/farmacologia
Indóis/farmacologia
Masculino
Oxirredução
Quercetina/farmacologia
Ácidos Quinolínicos/farmacologia
Coelhos
Ratos
Ratos Wistar
Espectrometria de Fluorescência
Espectrofotometria Atômica
Álcoois Açúcares/farmacologia
Reagentes de Sulfidrila/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amides); 0 (Arsenates); 0 (Arsenites); 0 (Bay W1807); 0 (Enzyme Inhibitors); 0 (Imino Furanoses); 0 (Indoles); 0 (Quinolinic Acids); 0 (Sugar Alcohols); 0 (Sulfhydryl Reagents); 0 (Xenobiotics); 100937-53-9 (1,4-dideoxy-1,4-iminoarabinitol); 3G6A5W338E (Caffeine); 415SHH325A (Adenosine Monophosphate); 56-73-5 (Glucose-6-Phosphate); 61D2G4IYVH (Adenosine Diphosphate); 7XO134LHLN (sodium arsenate); 8L70Q75FXE (Adenosine Triphosphate); 9005-79-2 (Glycogen); 9IKM0I5T1E (Quercetin); B40ROO395Z (Arabinose); EC 2.4.1.- (Glycogen Phosphorylase, Liver Form); EC 2.4.1.- (Glycogen Phosphorylase, Muscle Form); FKX709RK3Q (CP 320626); GAN16C9B8O (Glutathione); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:0712
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070819
[St] Status:MEDLINE


  9 / 523 MEDLINE  
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[PMID]:17600080
[Au] Autor:Prunier AL; Schuch R; Fernández RE; Mumy KL; Kohler H; McCormick BA; Maurelli AT
[Ad] Endereço:Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Bethesda, MD 20814-4799, USA.
[Ti] Título:nadA and nadB of Shigella flexneri 5a are antivirulence loci responsible for the synthesis of quinolinate, a small molecule inhibitor of Shigella pathogenicity.
[So] Source:Microbiology;153(Pt 7):2363-72, 2007 Jul.
[Is] ISSN:1350-0872
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The evolution of bacterial pathogens from commensal organisms involves virulence gene acquisition followed by pathoadaptation to the new host, including inactivation of antivirulence loci (AVL). AVL are core ancestral genes whose expression is incompatible with the pathogenic lifestyle. Previous studies identified cadA (encoding lysine decarboxylase) as an AVL of Shigella spp. In this study, AVL of Shigella were identified by examining a phenotypic difference from its non-pathogenic ancestor, Escherichia coli. Unlike most E. coli strains, Shigella spp. are nicotinic acid auxotrophs, the pathway for the de novo synthesis of NAD being uniformly defective. In Shigella flexneri, this defect is due to alterations in the nadA and/or nadB genes encoding the enzyme complex that converts L-aspartate to quinolinate, a precursor to NAD synthesis. Quinolinate was found to inhibit invasion and cell-to-cell spread of Sh. flexneri 5a and its ability to induce polymorphonuclear neutrophil transepithelial migration. Virulence of other Shigella species was also inhibited by quinolinate. Introduction of functional nadA and nadB genes from E. coli K-12 into Sh. flexneri 5a restored its ability to synthesize quinolinate but also resulted in strong attenuation of virulence in this strain. The results define nadA and nadB as AVL in Shigella and validate the concept of pathoadaptive evolution of bacteria from commensal ancestors by inactivation of AVL. They also suggest that studies focusing on this form of bacterial evolution can identify novel inhibitors of virulence in other bacterial pathogens.
[Mh] Termos MeSH primário: NAD/biossíntese
NAD/genética
Ácidos Quinolínicos/farmacologia
Shigella flexneri/patogenicidade
Virulência/genética
[Mh] Termos MeSH secundário: Genes Bacterianos
Células HeLa
Seres Humanos
Ácidos Quinolínicos/metabolismo
Shigella flexneri/genética
Virulência/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Quinolinic Acids); 0U46U6E8UK (NAD)
[Em] Mês de entrada:0711
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070630
[St] Status:MEDLINE


  10 / 523 MEDLINE  
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[PMID]:16619313
[Au] Autor:Montes VA; Pohl R; Shinar J; Anzenbacher P
[Ad] Endereço:Department of Chemistry and Center for Photochemical Sciences, Bowling Green State University (BGSU), Bowling Green, OH 43403, USA.
[Ti] Título:Effective manipulation of the electronic effects and its influence on the emission of 5-substituted tris(8-quinolinolate) aluminum(III) complexes.
[So] Source:Chemistry;12(17):4523-35, 2006 Jun 02.
[Is] ISSN:0947-6539
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The unique electron-transport and emissive properties of tris(8-quinolinolate) aluminum(III) (Alq(3)) have resulted in extensive use of this material for small molecular organic light-emitting diode (OLED) fabrication. So far, efforts to prepare stable and easy-to-process red/green/blue (RGB)-emitting Alq(3) derivatives have met with only a limited success. In this paper, we describe how the electronic nature of various substituents, projected via an arylethynyl or aryl spacer to the position of the highest HOMO density (C5), may be used for effective emission tuning to obtain blue-, green-, and red-emitting materials. The synthetic strategy consists of four different pathways for the attachment of electron-donating and electron-withdrawing aryl or arylethynyl substituents to the 5-position of the quinolinolate ring. Successful tuning of the emission color covering the whole visible spectrum (lambda=450-800 nm) was achieved. In addition, the photophysical properties of the luminophores were found to correlate with the Hammett constant of the respective substituents, providing a powerful strategy with which to predict the optical properties of new materials. We also demonstrate that the electronic nature of the substituent affects the emission properties of the resulting complex through effective modification of the HOMO levels of the quinolinolate ligand.
[Mh] Termos MeSH primário: Alumínio/química
Elétrons
Compostos Organometálicos/química
Ácidos Quinolínicos/química
[Mh] Termos MeSH secundário: Eletroquímica
Transporte de Elétrons
Luz
Compostos Organometálicos/síntese química
Ácidos Quinolínicos/síntese química
Semicondutores
Análise Espectral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Organometallic Compounds); 0 (Quinolinic Acids); CPD4NFA903 (Aluminum)
[Em] Mês de entrada:0707
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060419
[St] Status:MEDLINE



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