Malonate

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You Qi Tang - One of the best experts on this subject based on the ideXlab platform.

Miguel Julve - One of the best experts on this subject based on the ideXlab platform.

  • Protonated Malonate: the influence of the hydrogen bonds on the magnetic behaviour
    CrystEngComm, 2004
    Co-Authors: Fernando S. Delgado, Joaquín Sanchiz, Catalina Ruiz-pérez, Francesc Lloret, Miguel Julve
    Abstract:

    One hydrogen malonato-bridged complex of formula [Cu(Hmal)2] (1) and two polymorphous malonato-bridged complexes of formula [Cu(H2O)(H2mal)(mal)] (2 and 3), in which the three species of the Malonate (H2mal, Hmal−, and mal2−) are present, were synthesised and characterized by X-ray diffraction [H2mal = malonic acid]. Their structures consist of corrugated Malonate layers of [Cu(Hmal)2] (1) and [Cu(H2O)(H2mal)(mal)] (2 and 3) units bridged by carboxylate–Malonate groups. The layers are linked through hydrogen bonds leading to a three-dimensional network. Variable-temperature (1.9–290 K) magnetic susceptibility measurements indicate the occurrence of weak ferromagnetic interactions between the copper(II) ions through the carboxylate–Malonate bridge. The effectiveness of magnetic exchange coupling is related to the degree of protonation of the Malonate group.

  • design of high dimensional copper ii Malonate complexes with exo polydentate n donor ligands
    Inorganic Chemistry, 2003
    Co-Authors: Fernando S. Delgado, Joaquín Sanchiz, Francesc Lloret, Catalina Ruizperez, Miguel Julve
    Abstract:

    Two polymeric malonato-bridged copper(II) complexes of formulas {(H2bpe)[Cu(mal)2]}n·4nH2O (1) and [Cu4(mal)4(bpe)3]n·6nH2O (2) [mal = Malonate dianion; bpe = 1,2-bis(4-pyridyl)ethylene] have been synthesized and characterized by X-ray diffraction. Complex 1 crystallizes in triclinic space group P1, Z = 1, with unit cell parameters a = 4.8831(10) A, b = 9.585(2) A, c = 11.813(2) A, α = 77.29(3)°, β = 82.18(3)°, and γ = 84.92(3)°, whereas complex 2 crystallizes in the monoclinic space group P21/n, Z = 4, with unit cell parameters a = 13.462(3) A, b = 10.275(5) A, c = 19.579(4) A, and β = 105.21(3)°. The structure of 1 consists of anionic malonato-bridged uniform copper(II) chains which are connected through hydrogen bonds involving Malonate-oxygen atoms, noncoordinated water molecules, and H2bpe2+ cations. The intrachain copper−copper separation through carboxylate-Malonate bridge in the anti−syn conformation is 4.8831(10) A. Complex 2 possesses a three-dimensional structure made up of neutral corrugated ...

  • magnetic coupling through the carbon skeleton of Malonate in two polymorphs of cu bpy h2o cu bpy mal h2o clo4 2 h2mal malonic acid bpy 2 2 bipyridine
    Inorganic Chemistry, 2000
    Co-Authors: Catalina Ruizperez, Francesc Lloret, Maria Hernandezmolina, Pablo Lorenzoluis, Juan Cano, Miguel Julve
    Abstract:

    Two polymorphic malonato-bridged copper(II) complexes of formula {[Cu(bpy)(H2O)][Cu(bpy)(mal)(H2O)]}(ClO4)2 (1 and 2) (bpy = 2,2‘-bipyridine and mal = Malonate dianion) have been prepared and their structures solved by X-ray diffraction methods. Compound 1 crystallizes in the monoclinic space group P21/a, with a = 23.743(3) A, b = 9.7522(5) A, c = 27.731(2) A, β = 114.580(10)°, and Z = 4. Compound 2 crystallizes in the orthorhombic space group Pbcn, with a = 23.700(5) A, b = 25.162(5) A, c = 9.693(5) A, and Z = 4. The structures of 1 and 2 are made up of uncoordinated perchlorate anions and Malonate-bridged zigzag copper(II) chains grouped in an isosceles triangle running parallel to the b (1) and c (2) axes. These chains are built by a [Cu(bpy)(mal)(H2O)] unit acting as bis-monodentate ligand toward two [Cu(bpy)(H2O)] adjacent units through its OCCCO skeleton in an anti−anti conformation, whereas the OCO carboxylate bridges exhibit the anti−syn conformation. Compounds 1 and 2 contain four crystallographi...

Yong Ge Wei - One of the best experts on this subject based on the ideXlab platform.

Antonio Rodriguezsinovas - One of the best experts on this subject based on the ideXlab platform.

  • selective inhibition of succinate dehydrogenase in reperfused myocardium with intracoronary Malonate reduces infarct size
    Scientific Reports, 2018
    Co-Authors: Laura Vallslacalle, Ignasi Barba, Elisabet Mirocasas, Marisol Ruizmeana, Antonio Rodriguezsinovas
    Abstract:

    Inhibition of succinate dehydrogenase (SDH) with Malonate during reperfusion reduces infarct size in isolated mice hearts submitted to global ischemia. However, Malonate has toxic effects that preclude its systemic administration in animals. Here we investigated the effect of intracoronary Malonate on infarct size in pigs submitted to transient coronary occlusion. Under baseline conditions, 50 mmol/L of intracoronary disodium Malonate, but not lower concentrations, transiently reduced systolic segment shortening in the region perfused by the left anterior descending coronary artery (LAD) in open-chest pigs. To assess the effects of SDH inhibition on reperfusion injury, saline or Malonate 10 mmol/L were selectively infused into the area at risk in 38 animals submitted to ischemia-reperfusion. Malonate improved systolic shortening in the area at risk two hours after 15 min of ischemia (0.18 ± 0.07 vs 0.00 ± 0.01 a.u., p = 0.025, n = 3). In animals submitted to 40 min of ischemia, Malonate reduced reactive oxygen species production (MitoSOX staining) during initial reperfusion and limited infarct size (36.46 ± 5.35 vs 59.62 ± 4.00%, p = 0.002, n = 11), without modifying reperfusion arrhythmias. In conclusion, inhibition of SDH with intracoronary Malonate during early reperfusion limits reperfusion injury and infarct size in pigs submitted to transient coronary occlusion without modifying reperfusion arrhythmias or contractile function in distant myocardium.

  • succinate dehydrogenase inhibition with Malonate during reperfusion reduces infarct size by preventing mitochondrial permeability transition
    Cardiovascular Research, 2016
    Co-Authors: Laura Vallslacalle, Ignasi Barba, Elisabet Mirocasas, Marisol Ruizmeana, Antonio Rodriguezsinovas, Juan Jose Alburquerquebejar, Marina Fuertesagudo, David Garciadorado
    Abstract:

    Aims Previous studies demonstrated that pre-treatment with Malonate, a reversible inhibitor of succinate dehydrogenase, given before ischaemia, reduces infarct size. However, it is unknown whether administration of Malonate may reduce reperfusion injury. Methods and results Isolated mice hearts were treated, under normoxic conditions, with increasing concentrations of disodium Malonate (0.03–30 mmol/L, n = 4). Malonate induced a concentration-dependent decrease in left ventricular developed pressure (LVdevP) (EC50 = 8.05 ± 2.11 mmol/L). In isolated hearts submitted to global ischaemia (35 min) followed by reperfusion (60 min), Malonate 3 mmol/L given only during the first 15 min of reperfusion reduced lactate dehydrogenase release (125.41 ± 16.82 vs. 189.20 ± 13.74 U/g dry tissue/15 min in controls, P = 0.015) and infarct size (24.57 ± 2.32 vs. 39.84 ± 2.78%, P = 0.001, n = 7–8 per group) and improved recovery of LVdevP (20.06 ± 3.82 vs 7.76 ± 2.53% of baseline LVdevP, P = 0.017). 1H NMR spectroscopy demonstrated marked changes in the metabolic profile of Malonate-treated hearts, including increased accumulation of succinate. Furthermore, Malonate reduced reactive oxygen species (ROS) production, as measured by MitoSOX staining in myocardial samples obtained after 5 min of reperfusion and in mitochondrial preparations from these samples, preserved mitochondrial respiration, and reduced mitochondrial permeabilization, assessed by calcein retention. Treatment with Malonate did not result in activation of RISK or SAFE signalling pathways in tissue extracts obtained 5 min after reperfusion. Conclusion Succinate dehydrogenase inhibition with Malonate at the onset of reperfusion reduces infarct size in isolated mice hearts through reduction in ROS production and mitochondrial permeability transition pore opening.

Laura Vallslacalle - One of the best experts on this subject based on the ideXlab platform.

  • selective inhibition of succinate dehydrogenase in reperfused myocardium with intracoronary Malonate reduces infarct size
    Scientific Reports, 2018
    Co-Authors: Laura Vallslacalle, Ignasi Barba, Elisabet Mirocasas, Marisol Ruizmeana, Antonio Rodriguezsinovas
    Abstract:

    Inhibition of succinate dehydrogenase (SDH) with Malonate during reperfusion reduces infarct size in isolated mice hearts submitted to global ischemia. However, Malonate has toxic effects that preclude its systemic administration in animals. Here we investigated the effect of intracoronary Malonate on infarct size in pigs submitted to transient coronary occlusion. Under baseline conditions, 50 mmol/L of intracoronary disodium Malonate, but not lower concentrations, transiently reduced systolic segment shortening in the region perfused by the left anterior descending coronary artery (LAD) in open-chest pigs. To assess the effects of SDH inhibition on reperfusion injury, saline or Malonate 10 mmol/L were selectively infused into the area at risk in 38 animals submitted to ischemia-reperfusion. Malonate improved systolic shortening in the area at risk two hours after 15 min of ischemia (0.18 ± 0.07 vs 0.00 ± 0.01 a.u., p = 0.025, n = 3). In animals submitted to 40 min of ischemia, Malonate reduced reactive oxygen species production (MitoSOX staining) during initial reperfusion and limited infarct size (36.46 ± 5.35 vs 59.62 ± 4.00%, p = 0.002, n = 11), without modifying reperfusion arrhythmias. In conclusion, inhibition of SDH with intracoronary Malonate during early reperfusion limits reperfusion injury and infarct size in pigs submitted to transient coronary occlusion without modifying reperfusion arrhythmias or contractile function in distant myocardium.

  • succinate dehydrogenase inhibition with Malonate during reperfusion reduces infarct size by preventing mitochondrial permeability transition
    Cardiovascular Research, 2016
    Co-Authors: Laura Vallslacalle, Ignasi Barba, Elisabet Mirocasas, Marisol Ruizmeana, Antonio Rodriguezsinovas, Juan Jose Alburquerquebejar, Marina Fuertesagudo, David Garciadorado
    Abstract:

    Aims Previous studies demonstrated that pre-treatment with Malonate, a reversible inhibitor of succinate dehydrogenase, given before ischaemia, reduces infarct size. However, it is unknown whether administration of Malonate may reduce reperfusion injury. Methods and results Isolated mice hearts were treated, under normoxic conditions, with increasing concentrations of disodium Malonate (0.03–30 mmol/L, n = 4). Malonate induced a concentration-dependent decrease in left ventricular developed pressure (LVdevP) (EC50 = 8.05 ± 2.11 mmol/L). In isolated hearts submitted to global ischaemia (35 min) followed by reperfusion (60 min), Malonate 3 mmol/L given only during the first 15 min of reperfusion reduced lactate dehydrogenase release (125.41 ± 16.82 vs. 189.20 ± 13.74 U/g dry tissue/15 min in controls, P = 0.015) and infarct size (24.57 ± 2.32 vs. 39.84 ± 2.78%, P = 0.001, n = 7–8 per group) and improved recovery of LVdevP (20.06 ± 3.82 vs 7.76 ± 2.53% of baseline LVdevP, P = 0.017). 1H NMR spectroscopy demonstrated marked changes in the metabolic profile of Malonate-treated hearts, including increased accumulation of succinate. Furthermore, Malonate reduced reactive oxygen species (ROS) production, as measured by MitoSOX staining in myocardial samples obtained after 5 min of reperfusion and in mitochondrial preparations from these samples, preserved mitochondrial respiration, and reduced mitochondrial permeabilization, assessed by calcein retention. Treatment with Malonate did not result in activation of RISK or SAFE signalling pathways in tissue extracts obtained 5 min after reperfusion. Conclusion Succinate dehydrogenase inhibition with Malonate at the onset of reperfusion reduces infarct size in isolated mice hearts through reduction in ROS production and mitochondrial permeability transition pore opening.