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Pesquisa : D02.691.750.100.710 [Categoria DeCS]
Referências encontradas : 347 [refinar]
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[PMID]:29223393
[Au] Autor:Korotkov SM; Konovalova SA; Nesterov VP; Brailovskaya IV
[Ad] Endereço:Sechenov Institute of Evolutionary Physiology and Biochemistry, The Russian Academy of Sciences, Thorez pr. 44, 194223 St. Petersburg, Russia. Electronic address: korotkov@SK1645.spb.edu.
[Ti] Título:Mersalyl prevents the Tl -induced permeability transition pore opening in the inner membrane of Ca -loaded rat liver mitochondria.
[So] Source:Biochem Biophys Res Commun;495(2):1716-1721, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It was earlier shown that the calcium load of rat liver mitochondria in medium containing TlNO and KNO resulted in the Tl -induced mitochondrial permeability transition pore (MPTP) opening in the inner membrane. This opening was accompanied by an increase in swelling and membrane potential dissipation and a decrease in state 3, state 4, and 2,4-dinitrophenol-uncoupled respiration. This respiratory decrease was markedly leveled by mersalyl (MSL), the phosphate symporter (PiC) inhibitor which poorly stimulated the calcium-induced swelling, but further increased the potential dissipation. All of these effects of Ca and MSL were visibly reduced in the presence of the MPTP inhibitors (ADP, N-ethylmaleimide, and cyclosporine A). High MSL concentrations attenuated the ability of ADP to inhibit the MPTP. Our data suggest that the PiC can participate in the Tl -induced MPTP opening in the inner membrane of Ca -loaded rat liver mitochondria.
[Mh] Termos MeSH primário: Mersalil/farmacologia
Mitocôndrias Hepáticas/efeitos dos fármacos
Mitocôndrias Hepáticas/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Tálio/farmacologia
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Técnicas In Vitro
Transporte de Íons/efeitos dos fármacos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Membranas Mitocondriais/efeitos dos fármacos
Membranas Mitocondriais/metabolismo
Dilatação Mitocondrial/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (mitochondrial permeability transition pore); 5X1IO031V8 (Mersalyl); AD84R52XLF (Thallium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


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[PMID]:23583906
[Au] Autor:Bobba A; Amadoro G; Petragallo VA; Calissano P; Atlante A
[Ad] Endereço:Institute of Biomembranes and Bioenergetics, CNR, Bari, Italy.
[Ti] Título:Dissecting the molecular mechanism by which NH2htau and Aß1-42 peptides impair mitochondrial ANT-1 in Alzheimer disease.
[So] Source:Biochim Biophys Acta;1827(7):848-60, 2013 Jul.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To find out whether and how the adenine nucleotide translocator-1 (ANT-1) inhibition due to NH2htau and Aß1-42 is due to an interplay between these two Alzheimer's peptides, ROS and ANT-1 thiols, use was made of mersalyl, a reversible alkylating agent of thiol groups that are oriented toward the external hydrophilic phase, to selectively block and protect, in a reversible manner, the -SH groups of ANT-1. The rate of ATP appearance outside mitochondria was measured as the increase in NADPH absorbance which occurs, following external addition of ADP, when ATP is produced by oxidative phosphorylation and exported from mitochondria in the presence of glucose, hexokinase and glucose-6-phosphate dehydrogenase. We found that the mitochondrial superoxide anions, whose production is induced at the level of Complex I by externally added Aß1-42 and whose release from mitochondria is significantly reduced by the addition of the VDAC inhibitor DIDS, modify the thiol group/s present at the active site of mitochondrial ANT-1, impair ANT-1 in a mersalyl-prevented manner and abrogate the toxic effect of NH2htau on ANT-1 when Aß1-42 is already present. A molecular mechanism is proposed in which the pathological Aß-NH2htau interplay on ANT-1 in Alzheimer's neurons involves the thiol redox state of ANT-1 and the Aß1-42-induced ROS increase. This result represents an important innovation because it suggests the possibility of using various strategies to protect cells at the mitochondrial level, by stabilizing or restoring mitochondrial function or by interfering with the energy metabolism providing a promising tool for treating or preventing AD.
[Mh] Termos MeSH primário: Translocador 1 do Nucleotídeo Adenina/metabolismo
Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/farmacologia
Cerebelo/metabolismo
Grânulos Citoplasmáticos/metabolismo
Mitocôndrias/metabolismo
Fragmentos de Peptídeos/farmacologia
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Células Cultivadas
Cerebelo/citologia
Metabolismo Energético
Inibidores Enzimáticos/farmacologia
Mersalil/farmacologia
Modelos Neurológicos
Consumo de Oxigênio
Polarografia
Ratos
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
Superóxidos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adenine Nucleotide Translocator 1); 0 (Amyloid beta-Peptides); 0 (Enzyme Inhibitors); 0 (Peptide Fragments); 0 (Reactive Oxygen Species); 0 (amyloid beta-protein (1-42)); 0 (tau Proteins); 11062-77-4 (Superoxides); 5X1IO031V8 (Mersalyl); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1308
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130416
[St] Status:MEDLINE


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[PMID]:21872567
[Au] Autor:Tepp K; Shevchuk I; Chekulayev V; Timohhina N; Kuznetsov AV; Guzun R; Saks V; Kaambre T
[Ad] Endereço:Laboratory of Bioenergetics, National Institute of Chemical Physics and Biophysics, Tallinn, Estonia.
[Ti] Título:High efficiency of energy flux controls within mitochondrial interactosome in cardiac intracellular energetic units.
[So] Source:Biochim Biophys Acta;1807(12):1549-61, 2011 Dec.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of our study was to analyze a distribution of metabolic flux controls of all mitochondrial complexes of ATP-Synthasome and mitochondrial creatine kinase (MtCK) in situ in permeabilized cardiac cells. For this we used their specific inhibitors to measure flux control coefficients (C(vi)(JATP)) in two different systems: A) direct stimulation of respiration by ADP and B) activation of respiration by coupled MtCK reaction in the presence of MgATP and creatine. In isolated mitochondria the C(vi)(JATP) were for system A: Complex I - 0.19, Complex III - 0.06, Complex IV 0.18, adenine nucleotide translocase (ANT) - 0.11, ATP synthase - 0.01, Pi carrier - 0.20, and the sum of C(vi)(JATP) was 0.75. In the presence of 10mM creatine (system B) the C(vi)(JATP) were 0.38 for ANT and 0.80 for MtCK. In the permeabilized cardiomyocytes inhibitors had to be added in much higher final concentration, and the following values of C(vi)(JATP) were determined for condition A and B, respectively: Complex I - 0.20 and 0.64, Complex III - 0.41 and 0.40, Complex IV - 0.40 and 0.49, ANT - 0.20 and 0.92, ATP synthase - 0.065 and 0.38, Pi carrier - 0.06 and 0.06, MtCK 0.95. The sum of C(vi)(JATP) was 1.33 and 3.84, respectively. Thus, C(vi)(JATP) were specifically increased under conditions B only for steps involved in ADP turnover and for Complex I in permeabilized cardiomyocytes within Mitochondrial Interactosome, a supercomplex consisting of MtCK, ATP-Synthasome, voltage dependent anion channel associated with tubulin ßII which restricts permeability of the mitochondrial outer membrane.
[Mh] Termos MeSH primário: Respiração Celular/fisiologia
Metabolismo Energético/fisiologia
Mitocôndrias/metabolismo
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Trifosfato de Adenosina/metabolismo
Animais
Antimicina A/análogos & derivados
Antimicina A/metabolismo
Atractilosídeo/análogos & derivados
Atractilosídeo/metabolismo
Creatina Quinase Mitocondrial/metabolismo
Dinitrofluorbenzeno/metabolismo
Inibidores Enzimáticos/metabolismo
Masculino
Mersalil/metabolismo
Translocases Mitocondriais de ADP e ATP/metabolismo
ATPases Mitocondriais Próton-Translocadoras/metabolismo
Modelos Teóricos
Miócitos Cardíacos/citologia
Consumo de Oxigênio
Ratos
Ratos Wistar
Rotenona/metabolismo
Cianeto de Sódio/metabolismo
Desacopladores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Uncoupling Agents); 03L9OT429T (Rotenone); 11118-72-2 (antimycin); 17754-44-8 (Atractyloside); 5X1IO031V8 (Mersalyl); 642-15-9 (Antimycin A); 8L70Q75FXE (Adenosine Triphosphate); 9068-80-8 (Mitochondrial ADP, ATP Translocases); D241E059U6 (Dinitrofluorobenzene); EC 2.7.3.2 (Creatine Kinase, Mitochondrial Form); EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases); O5DDB9Z95G (Sodium Cyanide); SNP1XL23E6 (carboxyatractyloside)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110830
[St] Status:MEDLINE
[do] DOI:10.1016/j.bbabio.2011.08.005


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[PMID]:20599776
[Au] Autor:Oppedisano F; Galluccio M; Indiveri C
[Ad] Endereço:Department of Cell Biology, University of Calabria, Via P.Bucci 4c, 87036 Arcavacata di Rende, Italy.
[Ti] Título:Inactivation by Hg2+ and methylmercury of the glutamine/amino acid transporter (ASCT2) reconstituted in liposomes: Prediction of the involvement of a CXXC motif by homology modelling.
[So] Source:Biochem Pharmacol;80(8):1266-73, 2010 Oct 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effect of HgCl(2), methylmercury and mersalyl on the glutamine/amino acid (ASCT2) transporter reconstituted in liposomes has been studied. Mercuric compounds externally added to the proteoliposomes, inhibited the glutamine/glutamine antiport catalyzed by the reconstituted transporter. Similar effects were observed by pre-treating the proteoliposomes with the mercurials and then removing unreacted compounds before the transport assay. The inhibition was reversed by DTE, cysteine and N-acetyl-cysteine but not by S-carboxymethyl-cysteine. The data demonstrated that the inhibition was due to covalent reaction of mercuric compounds with Cys residue(s) of the transporter. The IC(50) of the transporter for HgCl(2), methylmercury and mersalyl, were 1.4+/-0.10, 2.4+/-0.16 or 3.1+/-0.19 microM, respectively. Kinetic studies of the inhibition showed that the reagents behaved as non-competitive inhibitor. The presence of glutamine or Na(+) during the incubation of the mercuric compounds with the proteoliposomes did not exerted any protective effect on the inhibition. None of the compounds was transported by the reconstituted transporter. A metal binding motif CXXC has been predicted as possible site of interaction of the mercuric compounds with the transporter on the basis of the homology structural model of ASCT2 obtained using the glutamate transporter homologue from Pyrococcus horikoshii as template.
[Mh] Termos MeSH primário: Sistema ASC de Transporte de Aminoácidos/antagonistas & inibidores
Lipossomos/química
Cloreto de Mercúrio/farmacologia
Mercúrio/farmacologia
Mersalil/farmacologia
Compostos de Metilmercúrio/farmacologia
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sistema ASC de Transporte de Aminoácidos/metabolismo
Sítios de Ligação
Transporte Biológico
Glutamina
Antígenos de Histocompatibilidade Menor
Modelos Moleculares
Ligação Proteica
Conformação Proteica
Sódio
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Transport System ASC); 0 (Liposomes); 0 (Methylmercury Compounds); 0 (Minor Histocompatibility Antigens); 0 (Slc1a5 protein, rat); 0RH81L854J (Glutamine); 53GH7MZT1R (Mercuric Chloride); 5X1IO031V8 (Mersalyl); 9NEZ333N27 (Sodium); FXS1BY2PGL (Mercury)
[Em] Mês de entrada:1010
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100706
[St] Status:MEDLINE
[do] DOI:10.1016/j.bcp.2010.06.032


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[PMID]:19995548
[Au] Autor:Gutiérrez-Aguilar M; Pérez-Martínez X; Chávez E; Uribe-Carvajal S
[Ad] Endereço:Depto de Bioquímica, Instituto de Fisiología Celular, UNAM, Mexico City, Mexico.
[Ti] Título:In Saccharomyces cerevisiae, the phosphate carrier is a component of the mitochondrial unselective channel.
[So] Source:Arch Biochem Biophys;494(2):184-91, 2010 Feb 15.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mitochondrial permeability transition (PT) involves the opening of a mitochondrial unselective channel (MUC) resulting in membrane depolarization and increased permeability to ions. PT has been observed in many, but not all eukaryotic species. In some species, PT has been linked to cell death, although other functions, such as matrix ion detoxification or regulation of the rate of oxygen consumption have been considered. The identification of the proteins constituting MUC would help understand the biochemistry and physiology of this channel. It has been suggested that the mitochondrial phosphate carrier is a structural component of MUC and we decided to test this in yeast mitochondria. Mersalyl inhibits the phosphate carrier and it has been reported that it also triggers PT. Mersalyl induced opening of the decavanadate-sensitive Yeast Mitochondrial Unselective Channel (YMUC). In isolated yeast mitochondria from a phosphate carrier-null strain the sensitivity to both phosphate and mersalyl was lost, although the permeability transition was still evoked by ATP in a decavanadate-sensitive fashion. Polyethylene glycol (PEG)-induced mitochondrial contraction results indicated that in mitochondria lacking the phosphate carrier the YMUC is smaller: complete contraction for mitochondria from the wild type and the mutant strains was achieved with 1.45 and 1.1 kDa PEGs, respectively. Also, as expected for a smaller channel titration with 1.1 kDa PEG evidenced a higher sensitivity in mitochondria from the mutant strain. The above data suggest that the phosphate carrier is the phosphate sensor in YMUC and contributes to the structure of this channel.
[Mh] Termos MeSH primário: Proteínas de Transporte de Fosfato/metabolismo
Canais de Potássio/metabolismo
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Animais
Mersalil/farmacologia
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Dilatação Mitocondrial/efeitos dos fármacos
Permeabilidade/efeitos dos fármacos
Proteínas de Transporte de Fosfato/antagonistas & inibidores
Fosfatos/metabolismo
Polietilenoglicóis/farmacologia
Canais de Potássio/química
Canais de Potássio/deficiência
Canais de Potássio/genética
Saccharomyces cerevisiae/citologia
Saccharomyces cerevisiae/efeitos dos fármacos
Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/química
Proteínas de Saccharomyces cerevisiae/genética
Deleção de Sequência
Vanadatos/farmacologia
Canais de Ânion Dependentes de Voltagem/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Phosphate Transport Proteins); 0 (Phosphates); 0 (Potassium Channels); 0 (Saccharomyces cerevisiae Proteins); 0 (Voltage-Dependent Anion Channels); 0 (YMUC potassium channel protein, S cerevisiae); 30IQX730WE (Polyethylene Glycols); 3WHH0066W5 (Vanadates); 5X1IO031V8 (Mersalyl)
[Em] Mês de entrada:1002
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091210
[St] Status:MEDLINE
[do] DOI:10.1016/j.abb.2009.12.002


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[PMID]:18511459
[Au] Autor:Laus MN; Soccio M; Trono D; Cattivelli L; Pastore D
[Ad] Endereço:Dipartimento di Scienze Agro-ambientali, Chimica e Difesa Vegetale, Facoltà di Agraria, Università degli Studi di Foggia, Via Napoli, 25, 71100 Foggia, Italy.
[Ti] Título:Plant inner membrane anion channel (PIMAC) function in plant mitochondria.
[So] Source:Plant Cell Physiol;49(7):1039-55, 2008 Jul.
[Is] ISSN:1471-9053
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:To date, the existence of the plant inner membrane anion channel (PIMAC) has been shown only in potato mitochondria, but its physiological role remains unclear. In this study, by means of swelling experiments in K(+) and ammonium salts, we characterize a PIMAC-like anion-conducting pathway in mitochondria from durum wheat (DWM), a monocotyledonous species phylogenetically far from potato. DWM were investigated since they possess a very active potassium channel (PmitoK(ATP)), so implying a very active matching anion uniport pathway and, possibly, a coordinated function. As in potato mitochondria, the electrophoretic uptake of chloride and succinate was inhibited by matrix [H(+)], propranolol, and tributyltin, and was insensitive to Mg(2+), N,N'-dicyclohexylcarbodiimide (DCCD) and mercurials, thus showing PIMAC's existence in DWM. PIMAC actively transports dicarboxylates, oxodicarboxylates, tricarboxylates and Pi. Interestingly, a novel mechanism of swelling in ammonium salts of isolated plant mitochondria is reported, based on electrophoretic anion uptake via PIMAC and ammonium uniport via PmitoK(ATP). PIMAC is inhibited by physiological compounds, such as ATP and free fatty acids, by high electrical membrane potential (Delta Psi), but not by acyl-CoAs or reactive oxygen species. PIMAC was found to cooperate with dicarboxylate carrier by allowing succinate uptake that triggers succinate/malate exchange in isolated DWM. Similar results were obtained using mitochondria from the dicotyledonous species topinambur, so suggesting generalization of results. We propose that PIMAC is normally inactive in vivo due to ATP and Delta Psi inhibition, but activation may occur in mitochondria de-energized by PmitoK(ATP) (or other dissipative systems) to replace or integrate the operation of classical anion carriers.
[Mh] Termos MeSH primário: Helianthus/metabolismo
Canais Iônicos/metabolismo
Mitocôndrias/metabolismo
Membranas Mitocondriais/metabolismo
Triticum/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/farmacologia
Carbonil Cianeto p-Trifluormetoxifenil Hidrazona/farmacologia
Ácidos Graxos/farmacologia
Helianthus/efeitos dos fármacos
Peróxido de Hidrogênio/farmacologia
Concentração de Íons de Hidrogênio/efeitos dos fármacos
Ácido Linoleico/farmacologia
Malatos/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mersalil/farmacologia
Mitocôndrias/efeitos dos fármacos
Membranas Mitocondriais/efeitos dos fármacos
Dilatação Mitocondrial/efeitos dos fármacos
NAD/farmacologia
Osmose/efeitos dos fármacos
Propranolol/farmacologia
Soluções
Ácido Succínico/metabolismo
Superóxidos/farmacologia
Triticum/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Ion Channels); 0 (Malates); 0 (Solutions); 0U46U6E8UK (NAD); 11062-77-4 (Superoxides); 370-86-5 (Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone); 5X1IO031V8 (Mersalyl); 817L1N4CKP (malic acid); 8L70Q75FXE (Adenosine Triphosphate); 9KJL21T0QJ (Linoleic Acid); 9Y8NXQ24VQ (Propranolol); AB6MNQ6J6L (Succinic Acid); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:0808
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080531
[St] Status:MEDLINE
[do] DOI:10.1093/pcp/pcn082


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[PMID]:17906363
[Au] Autor:García N; Martínez-Abundis E; Pavón N; Chávez E
[Ad] Endereço:Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Juan Badiano # 1, Col. Sección XVI, Tlalpam, Mexico, DF, 014080, Mexico. ngarciar@salud.gob.mx
[Ti] Título:On the opening of an insensitive cyclosporin A non-specific pore by phenylarsine plus mersalyl.
[So] Source:Cell Biochem Biophys;49(2):84-90, 2007.
[Is] ISSN:1085-9195
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this work was addressed to provide new information on the effect of thiol reagents on mitochondrial non-specific pore opening, and its response to cyclosporin A (CSA). To meet this proposal phenylarsine oxide (PHA) and mersalyl were employed as tools to induce permeability transition and CSA to inhibit it. PHA-induced mitochondrial dysfunction, characterized by Ca2+ efflux, swelling, and membrane de-energization, was inhibited by N-ethylmaleimide and CSA. Conversely, mersalyl failed to inhibit the inducing effect of phenylarsine oxide, it rather strengthened it. In addition, the effect of mersalyl was associated with cross-linking of membrane proteins. The content of membrane thiol groups accessible to react with PHA, mersalyl, and PHA plus mersalyl was determined. In all situations, permeability transition was accompanied by a significant decrease in the whole free membrane thiol content. Interestingly, it is also shown that mersalyl hinders the protective effect of cyclosporin A on PHA-induced matrix Ca2+ efflux.
[Mh] Termos MeSH primário: Arsenicais/farmacologia
Ciclosporina/farmacologia
Ativação do Canal Iônico/efeitos dos fármacos
Mersalil/farmacologia
Membranas Mitocondriais/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Reagentes para Ligações Cruzadas
Etilmaleimida/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Mitocôndrias Hepáticas/metabolismo
Translocases Mitocondriais de ADP e ATP/metabolismo
Membranas Mitocondriais/efeitos dos fármacos
Dilatação Mitocondrial/efeitos dos fármacos
Permeabilidade/efeitos dos fármacos
Porinas/metabolismo
Ligação Proteica/efeitos dos fármacos
Ratos
Compostos de Sulfidrila/química
Reagentes de Sulfidrila/química
Reagentes de Sulfidrila/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arsenicals); 0 (Cross-Linking Reagents); 0 (Porins); 0 (Sulfhydryl Compounds); 0 (Sulfhydryl Reagents); 0HUR2WY345 (oxophenylarsine); 5X1IO031V8 (Mersalyl); 83HN0GTJ6D (Cyclosporine); 9068-80-8 (Mitochondrial ADP, ATP Translocases); O3C74ACM9V (Ethylmaleimide); SY7Q814VUP (Calcium)
[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:071002
[St] Status:MEDLINE


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[PMID]:17485229
[Au] Autor:García N; Martínez-Abundis E; Pavón N; Correa F; Chávez E
[Ad] Endereço:Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Juan Badiano # 1, Tlalpam, DF 014080, México.
[Ti] Título:Copper induces permeability transition through its interaction with the adenine nucleotide translocase.
[So] Source:Cell Biol Int;31(9):893-9, 2007 Sep.
[Is] ISSN:1065-6995
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this work we examined the effect of low concentrations of Cu(2+) on the opening of the mitochondrial non-specific pore. The purpose was addressed to further contribute to the knowledge of the mechanisms that regulate the open/closed cycles of the permeability transition pore. Membrane leakage was established by measuring matrix Ca(2+) efflux and mitochondrial swelling. The experimental results indicate that Cu(2+) at very low concentrations promoted the release of accumulated Ca(2+), as well as mitochondrial swelling, provided 1,10-phenanthroline has been added. Carboxyatractyloside and Cu(2+) exhibited additive effects on these parameters. After Cu(2+) titration of membrane thiols, it might be assumed that the blockage of 5.9nmol of SH/mg protein suffices to open the non-specific pore. Taking into account the reinforcing effect of carboxyatractyloside, the increasing ADP concentrations, and that N-ethylmaleimide inhibited the Cu(2+)-induced Ca(2+) efflux, it is proposed that the target site for Cu(2+) is located in the ADP/ATP carrier.
[Mh] Termos MeSH primário: Cobre/farmacologia
Translocases Mitocondriais de ADP e ATP/metabolismo
[Mh] Termos MeSH secundário: Difosfato de Adenosina/farmacologia
Animais
Atractilosídeo/análogos & derivados
Atractilosídeo/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Etilmaleimida/farmacologia
Glutationa/metabolismo
Mersalil/farmacologia
Membranas Mitocondriais/efeitos dos fármacos
Proteínas Mitocondriais/isolamento & purificação
Dilatação Mitocondrial/efeitos dos fármacos
Permeabilidade/efeitos dos fármacos
Ratos
Compostos de Sulfidrila/metabolismo
Titulometria
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (Sulfhydryl Compounds); 17754-44-8 (Atractyloside); 5X1IO031V8 (Mersalyl); 61D2G4IYVH (Adenosine Diphosphate); 789U1901C5 (Copper); 9068-80-8 (Mitochondrial ADP, ATP Translocases); GAN16C9B8O (Glutathione); O3C74ACM9V (Ethylmaleimide); SNP1XL23E6 (carboxyatractyloside)
[Em] Mês de entrada:0708
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070509
[St] Status:MEDLINE


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[PMID]:17011537
[Au] Autor:Letelier ME; Martínez M; González-Lira V; Faúndez M; Aracena-Parks P
[Ad] Endereço:Laboratory of Pharmacology, Department of Pharmacological and Toxicological Chemistry, Chemical and Pharmaceutical Sciences School, Universidad de Chile, Olivos 1007, Independencia, Santiago, Chile. mel@ciq.uchile.cl
[Ti] Título:Inhibition of cytosolic glutathione S-transferase activity from rat liver by copper.
[So] Source:Chem Biol Interact;164(1-2):39-48, 2006 Dec 01.
[Is] ISSN:0009-2797
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:H(2)O(2) inactivation of particular GST isoforms has been reported, with no information regarding the overall effect of other ROS on cytosolic GST activity. The present work describes the inactivation of total cytosolic GST activity from liver rats by the oxygen radical-generating system Cu(2+)/ascorbate. We have previously shown that this system may change some enzymatic activities of thiol proteins through two mechanisms: ROS-induced oxidation and non-specific Cu(2+) binding to protein thiol groups. In the present study, we show that nanomolar Cu(2+) in the absence of ascorbate did not modify total cytosolic GST activity; the same concentrations of Cu(2+) in the presence of ascorbate, however, inhibited this activity. Micromolar Cu(2+) in either the absence or presence of ascorbate inhibited cytosolic GST activity. Kinetic studies show that GSH but no 1-chloro-2,4-dinitrobenzene prevent the inhibition on cytosolic GST induced by micromolar Cu(2+) either in the absence or presence of ascorbate. On the other hand, NEM and mersalyl acid, both thiol-alkylating agents, inhibited GST activity with differential reactivity in a dose-dependent manner. Taken together, these results suggest that an inhibitory Cu(2+)-binding effect is likely to be negligible on the overall inhibition of cytosolic GST activity observed by the Cu(2+)/ascorbate system. We discuss how modification of GST-thiol groups is related to the inhibition of cytosolic GST activity.
[Mh] Termos MeSH primário: Ácido Ascórbico/farmacologia
Cobre/farmacologia
Citosol/metabolismo
Inibidores Enzimáticos/farmacologia
Glutationa Transferase/antagonistas & inibidores
Fígado/metabolismo
[Mh] Termos MeSH secundário: Alquilantes/farmacologia
Animais
Sítios de Ligação
Dinitroclorobenzeno/farmacologia
Relação Dose-Resposta a Droga
Cinética
Fígado/ultraestrutura
Masculino
Mersalil/farmacologia
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Compostos de Sulfidrila/química
Compostos de Sulfidrila/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Enzyme Inhibitors); 0 (Reactive Oxygen Species); 0 (Sulfhydryl Compounds); 5X1IO031V8 (Mersalyl); 789U1901C5 (Copper); EC 2.5.1.18 (Glutathione Transferase); GE3IBT7BMN (Dinitrochlorobenzene); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:0701
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061003
[St] Status:MEDLINE


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[PMID]:16760707
[Au] Autor:Ventura HO
[Ad] Endereço:Department of Cardiology, Ochsner Clinic Foundation, New Orleans, LA, USA.
[Ti] Título:History of heart failure.
[So] Source:Congest Heart Fail;12(3):178, 2006 May-Jun.
[Is] ISSN:1527-5299
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Barbitúricos/história
Diuréticos/história
Insuficiência Cardíaca/história
Mersalil/história
[Mh] Termos MeSH secundário: Barbitúricos/efeitos adversos
Diuréticos/efeitos adversos
Insuficiência Cardíaca/tratamento farmacológico
História do Século XX
Seres Humanos
Mersalil/efeitos adversos
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Barbiturates); 0 (Diuretics); 2LN1O9240E (merbaphen); 5X1IO031V8 (Mersalyl)
[Em] Mês de entrada:0607
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060609
[St] Status:MEDLINE



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