The Experts below are selected from a list of 510 Experts worldwide ranked by ideXlab platform
Chengchin Kuo - One of the best experts on this subject based on the ideXlab platform.
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Vanadium Derivative exposure promotes functional alterations of vsmcs and consequent atherosclerosis via ros p38 nf κb mediated il 6 production
International Journal of Molecular Sciences, 2019Co-Authors: Changching Yeh, Guanlin Lee, Hsiuting Wen, Pinpin Lin, Chengchin KuoAbstract:Vanadium is a transition metal widely distributed in the Earth's crust, and is a major contaminant in fossil fuels. Its pathological effect and regulation in atherosclerosis remain unclear. We found that intranasal administration of the Vanadium Derivative NaVO3 significantly increased plasma and urinary Vanadium levels and induced arterial lipid accumulation and atherosclerotic lesions in apolipoprotein E-deficient knockout mice (ApoE-/-) murine aorta compared to those in vehicle-exposed mice. This was accompanied by an increase in plasma reactive oxygen species (ROS) and interleukin 6 (IL-6) levels and a decrease in the vascular smooth muscle cell (VSMC) differentiation marker protein SM22α in the atherosclerotic lesions. Furthermore, exposure to NaVO3 or VOSO4 induced cytosolic ROS generation and IL-6 production in VSMCs and promoted VSMC synthetic differentiation, migration, and proliferation. The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice. Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-κB-dependent pathways. Neutralizing anti-IL-6 antibodies impaired NaVO3-mediated VSMC migration and proliferation. We concluded that NaVO3 exposure activates the ROS-triggering p38 signaling to selectively induce NF-κB-mediated IL-6 production. These signaling pathways induce VSMC synthetic differentiation, migration, and proliferation, leading to lipid accumulation and atherosclerosis.
Georgiy B Shulpin - One of the best experts on this subject based on the ideXlab platform.
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oxidations by the reagent o2 h2o2 Vanadium Derivative pyrazine 2 carboxylic acid part 14 competitive oxidation of alkanes and acetonitrile solvent
Journal of Molecular Catalysis A-chemical, 2005Co-Authors: Yuriy N Kozlov, G V Nizova, Georgiy B ShulpinAbstract:Abstract It has been found that the rate of hydrogen peroxide consumption in an alkane oxidation by the “O2–H2O2–nBu4NVO3–pyrazine-2-carboxylic acid” reagent in acetonitrile is noticeably lower in the presence of an alkane than in its absence. This paradoxical phenomenon at the first glance can be explained if we assume that acetonitrile used as a solvent is efficiently oxidized by the system in the absence of alkane. This oxidation is depressed by alkane additive due to the competition between the alkane and acetonitrile for the active hydroxyl radicals efficiently generated by the reagent. It has been also shown that the H2O2 decomposition in the presence of an alkane occurs as a radical non-chain process.
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oxidations by the reagent o2 h2o2 Vanadium Derivative pyrazine 2 carboxylic acid part 13 kinetics and mechanism of the benzene hydroxylation
New Journal of Chemistry, 2003Co-Authors: Marcus H C De La Cruz, Yuriy N Kozlov, Elizabeth R Lachter, Georgiy B ShulpinAbstract:It has been concluded on the basis of the kinetic study of benzene hydroxylation by the “O2–H2O2–nBu4NVO3–PCA” reagent in acetonitrile at various temperatures that the oxidation is induced by the attack of hydroxyl radical on the benzene molecule. The rate-limiting step of the reaction is the monomolecular decomposition of the complex containing one coordinated PCA molecule as well as one hydrogen peroxide molecule: VV(PCA)(H2O2) → VIV(PCA) + HOO˙ + H+. The V(IV) species thus formed reacts further in a non-limiting stage with the second H2O2 molecule to generate the hydroxyl radical: VIV(PCA) + H2O2 → VV(PCA) + HO˙ + HO−. The effective activation energy is 19 ± 3 kcal mol−1.
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oxidations by the reagent o2 h2o2 Vanadium Derivative pyrazine 2 carboxylic acid part 12 1 main features kinetics and mechanism of alkane hydroperoxidation
Journal of The Chemical Society-perkin Transactions 1, 2001Co-Authors: Georgiy B Shulpin, Yuriy N Kozlov, G V Nizova, Georg Sussfink, Sandrine Stanislas, Alex Kitaygorodskiy, Vera S KulikovaAbstract:Various combinations of Vanadium Derivatives (n-Bu4NVO3 is the best catalyst) with pyrazine-2-carboxylic acid (PCA) catalyse the oxidation of saturated hydrocarbons, RH, with hydrogen peroxide and air in acetonitrile solution to produce, at temperatures <40 °C, alkyl hydroperoxides, ROOH, as the main primary products. These compounds are easily reduced with triphenylphosphine to the corresponding alcohols, which can then be quantitatively determined by GLC. Certain aminoacids similar to PCA can play the role of co-catalyst; however the oxidation rates and final product yields are lower for picolinic and imidazole-4,5-dicarboxylic acids, while imidazole-4-carboxylic and pyrazole-3,5-dicarboxylic acids are almost inactive. The oxidation is induced by the attack of a hydroxyl radical on the alkane, RH, to produce alkyl radicals, R˙. The latter further react rapidly with molecular atmospheric oxygen. The peroxyl radicals, ROO˙, thus formed can be converted to alkyl hydroperoxides. We conclude on the basis of our kinetic investigation of the oxidation of cyclohexane that the rate-limiting step of the reaction is the monomolecular decomposition of the complex containing one coordinated PCA molecule: VV(PCA)(H2O2) → VIV(PCA) + HOO˙ + H+. The VIV species thus formed reacts further with a second H2O2 molecule to generate the hydroxyl radical according to the equation VIV(PCA) + H2O2 → VV(PCA) + HO˙ + HO−. The concentration of the active species in the course of the catalytic process has been estimated to be as low as [V(PCA)H2O2] ≊ 3.3 × 10−6 mol dm−3. The effective rate constant for the cyclohexane oxidation (d[ROOH]/dt = keff[H2O2]0[V]0) is keff = 0.44 dm3 mol−1 s−1 at 40 °C, the effective activation energy is 17 ± 2 kcal mol−1. It is assumed that the accelerating role of PCA is due to its facilitating the proton transfer between the oxo and hydroxy ligands of the Vanadium complex on the one hand and molecules of hydrogen peroxide and water on the other hand. For example: (pca)(O)V⋯H2O2 → (pca)(HO–)V–OOH. Such a “robot’s arm mechanism” has analogies in enzyme catalysis.
Yuriy N Kozlov - One of the best experts on this subject based on the ideXlab platform.
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oxidations by the reagent o2 h2o2 Vanadium Derivative pyrazine 2 carboxylic acid part 14 competitive oxidation of alkanes and acetonitrile solvent
Journal of Molecular Catalysis A-chemical, 2005Co-Authors: Yuriy N Kozlov, G V Nizova, Georgiy B ShulpinAbstract:Abstract It has been found that the rate of hydrogen peroxide consumption in an alkane oxidation by the “O2–H2O2–nBu4NVO3–pyrazine-2-carboxylic acid” reagent in acetonitrile is noticeably lower in the presence of an alkane than in its absence. This paradoxical phenomenon at the first glance can be explained if we assume that acetonitrile used as a solvent is efficiently oxidized by the system in the absence of alkane. This oxidation is depressed by alkane additive due to the competition between the alkane and acetonitrile for the active hydroxyl radicals efficiently generated by the reagent. It has been also shown that the H2O2 decomposition in the presence of an alkane occurs as a radical non-chain process.
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oxidations by the reagent o2 h2o2 Vanadium Derivative pyrazine 2 carboxylic acid part 13 kinetics and mechanism of the benzene hydroxylation
New Journal of Chemistry, 2003Co-Authors: Marcus H C De La Cruz, Yuriy N Kozlov, Elizabeth R Lachter, Georgiy B ShulpinAbstract:It has been concluded on the basis of the kinetic study of benzene hydroxylation by the “O2–H2O2–nBu4NVO3–PCA” reagent in acetonitrile at various temperatures that the oxidation is induced by the attack of hydroxyl radical on the benzene molecule. The rate-limiting step of the reaction is the monomolecular decomposition of the complex containing one coordinated PCA molecule as well as one hydrogen peroxide molecule: VV(PCA)(H2O2) → VIV(PCA) + HOO˙ + H+. The V(IV) species thus formed reacts further in a non-limiting stage with the second H2O2 molecule to generate the hydroxyl radical: VIV(PCA) + H2O2 → VV(PCA) + HO˙ + HO−. The effective activation energy is 19 ± 3 kcal mol−1.
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oxidations by the reagent o2 h2o2 Vanadium Derivative pyrazine 2 carboxylic acid part 12 1 main features kinetics and mechanism of alkane hydroperoxidation
Journal of The Chemical Society-perkin Transactions 1, 2001Co-Authors: Georgiy B Shulpin, Yuriy N Kozlov, G V Nizova, Georg Sussfink, Sandrine Stanislas, Alex Kitaygorodskiy, Vera S KulikovaAbstract:Various combinations of Vanadium Derivatives (n-Bu4NVO3 is the best catalyst) with pyrazine-2-carboxylic acid (PCA) catalyse the oxidation of saturated hydrocarbons, RH, with hydrogen peroxide and air in acetonitrile solution to produce, at temperatures <40 °C, alkyl hydroperoxides, ROOH, as the main primary products. These compounds are easily reduced with triphenylphosphine to the corresponding alcohols, which can then be quantitatively determined by GLC. Certain aminoacids similar to PCA can play the role of co-catalyst; however the oxidation rates and final product yields are lower for picolinic and imidazole-4,5-dicarboxylic acids, while imidazole-4-carboxylic and pyrazole-3,5-dicarboxylic acids are almost inactive. The oxidation is induced by the attack of a hydroxyl radical on the alkane, RH, to produce alkyl radicals, R˙. The latter further react rapidly with molecular atmospheric oxygen. The peroxyl radicals, ROO˙, thus formed can be converted to alkyl hydroperoxides. We conclude on the basis of our kinetic investigation of the oxidation of cyclohexane that the rate-limiting step of the reaction is the monomolecular decomposition of the complex containing one coordinated PCA molecule: VV(PCA)(H2O2) → VIV(PCA) + HOO˙ + H+. The VIV species thus formed reacts further with a second H2O2 molecule to generate the hydroxyl radical according to the equation VIV(PCA) + H2O2 → VV(PCA) + HO˙ + HO−. The concentration of the active species in the course of the catalytic process has been estimated to be as low as [V(PCA)H2O2] ≊ 3.3 × 10−6 mol dm−3. The effective rate constant for the cyclohexane oxidation (d[ROOH]/dt = keff[H2O2]0[V]0) is keff = 0.44 dm3 mol−1 s−1 at 40 °C, the effective activation energy is 17 ± 2 kcal mol−1. It is assumed that the accelerating role of PCA is due to its facilitating the proton transfer between the oxo and hydroxy ligands of the Vanadium complex on the one hand and molecules of hydrogen peroxide and water on the other hand. For example: (pca)(O)V⋯H2O2 → (pca)(HO–)V–OOH. Such a “robot’s arm mechanism” has analogies in enzyme catalysis.
Changching Yeh - One of the best experts on this subject based on the ideXlab platform.
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Vanadium Derivative exposure promotes functional alterations of vsmcs and consequent atherosclerosis via ros p38 nf κb mediated il 6 production
International Journal of Molecular Sciences, 2019Co-Authors: Changching Yeh, Guanlin Lee, Hsiuting Wen, Pinpin Lin, Chengchin KuoAbstract:Vanadium is a transition metal widely distributed in the Earth's crust, and is a major contaminant in fossil fuels. Its pathological effect and regulation in atherosclerosis remain unclear. We found that intranasal administration of the Vanadium Derivative NaVO3 significantly increased plasma and urinary Vanadium levels and induced arterial lipid accumulation and atherosclerotic lesions in apolipoprotein E-deficient knockout mice (ApoE-/-) murine aorta compared to those in vehicle-exposed mice. This was accompanied by an increase in plasma reactive oxygen species (ROS) and interleukin 6 (IL-6) levels and a decrease in the vascular smooth muscle cell (VSMC) differentiation marker protein SM22α in the atherosclerotic lesions. Furthermore, exposure to NaVO3 or VOSO4 induced cytosolic ROS generation and IL-6 production in VSMCs and promoted VSMC synthetic differentiation, migration, and proliferation. The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice. Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-κB-dependent pathways. Neutralizing anti-IL-6 antibodies impaired NaVO3-mediated VSMC migration and proliferation. We concluded that NaVO3 exposure activates the ROS-triggering p38 signaling to selectively induce NF-κB-mediated IL-6 production. These signaling pathways induce VSMC synthetic differentiation, migration, and proliferation, leading to lipid accumulation and atherosclerosis.
Hsiuting Wen - One of the best experts on this subject based on the ideXlab platform.
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Vanadium Derivative exposure promotes functional alterations of vsmcs and consequent atherosclerosis via ros p38 nf κb mediated il 6 production
International Journal of Molecular Sciences, 2019Co-Authors: Changching Yeh, Guanlin Lee, Hsiuting Wen, Pinpin Lin, Chengchin KuoAbstract:Vanadium is a transition metal widely distributed in the Earth's crust, and is a major contaminant in fossil fuels. Its pathological effect and regulation in atherosclerosis remain unclear. We found that intranasal administration of the Vanadium Derivative NaVO3 significantly increased plasma and urinary Vanadium levels and induced arterial lipid accumulation and atherosclerotic lesions in apolipoprotein E-deficient knockout mice (ApoE-/-) murine aorta compared to those in vehicle-exposed mice. This was accompanied by an increase in plasma reactive oxygen species (ROS) and interleukin 6 (IL-6) levels and a decrease in the vascular smooth muscle cell (VSMC) differentiation marker protein SM22α in the atherosclerotic lesions. Furthermore, exposure to NaVO3 or VOSO4 induced cytosolic ROS generation and IL-6 production in VSMCs and promoted VSMC synthetic differentiation, migration, and proliferation. The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice. Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-κB-dependent pathways. Neutralizing anti-IL-6 antibodies impaired NaVO3-mediated VSMC migration and proliferation. We concluded that NaVO3 exposure activates the ROS-triggering p38 signaling to selectively induce NF-κB-mediated IL-6 production. These signaling pathways induce VSMC synthetic differentiation, migration, and proliferation, leading to lipid accumulation and atherosclerosis.
