Adrenochrome

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Alexander I Konovalov - One of the best experts on this subject based on the ideXlab platform.

  • Effect of silica coating and further silica surface decoration by phospholipid bilayer on quenching of Tb(III) complexes by Adrenochrome
    Journal of Molecular Liquids, 2015
    Co-Authors: Alsu R. Mukhametshina, Asiya R. Mustafina, Rustem Amirov, Konstantin A. Petrov, Victor V. Syakaev, Alexander I Konovalov
    Abstract:

    Abstract The present report introduces regularities and mechanisms of Tb(III)-centered luminescence quenching by Adrenochrome for Tb(III)-p-sulfonatothiacalix[4]arene complexes in the aqueous solutions and the same complexes doped into silica nanoparticles. The choice of Adrenochrome (the oxidized form of adrenaline) as quencher originates from its quenching effect on the Tb(III)-centered luminescence, which discriminates it from adrenaline and dopamine. The quenching through dynamic mechanism of the Tb(III) complexes in the solutions results from their concentration induced collision with Adrenochrome molecules. The quenching of the Tb(III)-doped silica nanoparticles also occurs through dynamic mechanism, although it is insignificant due to the shielding effect of the silica surface. The inclusion of the Tb(III)-doped silica nanoparticles into phospholipid bilayers influences the quenching of the Tb(III)-centered luminescence by Adrenochrome due to its binding with the bilayers deposited onto silica nanoparticles.

W. Klaus - One of the best experts on this subject based on the ideXlab platform.

  • Studies on the role of superoxide anion radicals for the cardiotoxicity of Adrenochrome.
    Drug Research, 2011
    Co-Authors: A. F. E. Rump, Kuno Güttler, R Rosen, Jörg Michael Schierholz, W. Klaus
    Abstract:

    Adrenochrome is an oxidative product of adrenaline and possesses cardiotoxic properties. As oxygen free radicals play a role in the cytotoxic effects of catecholamines, the role of superoxide anion radicals, as mediators of Adrenochrome toxicity, was investigated using electrically-driven Langendorff rabbit hearts with depleted catecholamine stores. Repetitive regional myocardial ischemia (MI) was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH-fluorescence photography. Adrenochrome (10 −4 mol/l) was added to the perfusion solution after a reperfusion period of 20 min, 30 min before the 2nd coronary occlusion, with or without the additional application of SOD (30 U/ml). Left ventricular pressure was significantly enhanced by Adrenochrome (p

  • Studies on the role of superoxide anion radicals for the cardiotoxicity of Adrenochrome.
    Arzneimittel-Forschung, 2011
    Co-Authors: A. F. E. Rump, Kuno Güttler, R Rosen, Jörg Michael Schierholz, W. Klaus
    Abstract:

    Adrenochrome is an oxidative product of adrenaline and possesses cardiotoxic properties. As oxygen free radicals play a role in the cytotoxic effects of catecholamines, the role of superoxide anion radicals, as mediators of Adrenochrome toxicity, was investigated using electrically-driven Langendorff rabbit hearts with depleted catecholamine stores. Repetitive regional myocardial ischemia (MI) was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH-fluorescence photography. Adrenochrome (10(-6) mol/l) was added to the perfusion solution after a reperfusion period of 20 min, 30 min before the 2nd coronary occlusion, with or without the additional application of SOD (30 U/ml). Left ventricular pressure was significantly enhanced by Adrenochrome (p < 0.05), but it fell rapidly down below its initial value (p < 0.05). Coronary flow was significantly decreased by Adrenochrome (p < 0.05). Whereas epicardial NADH-fluorescence was similar after repetitive coronary occlusions in untreated controls, it was significantly enhanced by Adrenochrome (p < 0.05). The deleterious effects of Adrenochrome on MI were not inhibited by SOD. Thus, there is no evidence for superoxide anion radicals as mediators of the deleterious effects of Adrenochrome on MI in isolated rabbit hearts. The deleterious effects of Adrenochrome on MI in isolated rabbit hearts might be caused by functional effects, impairing the oxygen consumption/oxygen supply balance.

  • Functional Effects of Adrenochrome in Isolated Rabbit Heart
    Pharmacology & Toxicology, 1995
    Co-Authors: A. F. E. Rump, W. Klaus
    Abstract:

    : The cardiotoxic effects of catecholamines have been explained in part by the generation of oxygen free radicals and aminochromes. The role of aminochromes remains however controversial. It has previously been demonstrated that Adrenochrome, an oxidation product of adrenaline, shows cardiotoxic properties only at very high concentrations, and it has been suggested that the deleterious effects observed may be caused by a worsening in myocardial perfusion. The functional properties of Adrenochrome were examined in isolated spontaneously-beating rabbit hearts with depleted catecholamine stores (reserpin 7.0 mg/kg 16-24 hr before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, [Ca++]sol. 1.8 mmol/l, 37 degrees). Cumulative concentration-response curves show an Adrenochrome-concentration-dependent increase of contractility (left ventricular pressure, EC50 = 3.6 x 10(-6) M; +dp/dtmax, EC50 = 1.6 x 10(-5) M), whereas myocardial relaxation was impaired (-dp/dtmax, EC50 = 2.6 x 10(-5) M; -dp/dtmax/+dp/dtmax = 0.68 at 10(-4) M). Heart-rate was only slightly enhanced (+10% at 10(-4) M), and the coronary flow was markedly influenced only by Adrenochrome 10(-4) M (-17%). The relative coronary flow (= global coronary flow/pressure-rate product) was concentration-dependently reduced (EC50 = 10(-5) M; -49% at 10(-4) M). We conclude that in isolated rabbit hearts, Adrenochrome has a positive inotropic action but impairs myocardial relaxation, and coronary constrictor activity prevents an increase of myocardial oxygen supply, thus worsening myocardial oxygen-demand/supply balance.

  • Cardiotoxicity of Adrenochrome in isolated rabbit hearts assessed by epicardial NADH fluorescence.
    Archives of Toxicology, 1994
    Co-Authors: A. F. E. Rump, W. Klaus
    Abstract:

    Noradrenaline in a micromolar concentration has recently been shown to contribute to ischemic tissue injury by direct cardiotoxic effects independent of functional alterations. Oxygen free radicals, generated during the auto-oxidation of catecholamines, are important mediators of catecholamine cardiotoxicity. However, the role of the oxidative products (aminochromes) is still unclear. We examined the effects of Adrenochrome on functional parameters and on regional myocardial ischemia (MI) in isolated electrically-driven rabbit hearts with depleted catecholamine stores (reserpine 7.0 mg/kg i.p. 16–24 h before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37°C). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH fluorescence photography. Adrenochrome-treatment (10−6 M or 10−4 M) was started after a reperfusion period of 20 min. The left ventricular pressure (LVP) was significantly enhanced by Adrenochrome (p 0.05), but it was significantly decreased by Adrenochrome 10−4 M (P 0.05) and more markedly by Adrenochrome 10−4 M (p 0.05), it was significantly enhanced by Adrenochrome 10−4 M (p

  • cardiotoxicity of Adrenochrome in isolated rabbit hearts assessed by epicardial nadh fluorescence
    Archives of Toxicology, 1994
    Co-Authors: A. F. E. Rump, W. Klaus
    Abstract:

    Noradrenaline in a micromolar concentration has recently been shown to contribute to ischemic tissue injury by direct cardiotoxic effects independent of functional alterations. Oxygen free radicals, generated during the auto-oxidation of catecholamines, are important mediators of catecholamine cardiotoxicity. However, the role of the oxidative products (aminochromes) is still unclear. We examined the effects of Adrenochrome on functional parameters and on regional myocardial ischemia (MI) in isolated electrically-driven rabbit hearts with depleted catecholamine stores (reserpine 7.0 mg/kg i.p. 16–24 h before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37°C). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH fluorescence photography. Adrenochrome-treatment (10−6 M or 10−4 M) was started after a reperfusion period of 20 min. The left ventricular pressure (LVP) was significantly enhanced by Adrenochrome (p 0.05), but it was significantly decreased by Adrenochrome 10−4 M (P 0.05) and more markedly by Adrenochrome 10−4 M (p 0.05), it was significantly enhanced by Adrenochrome 10−4 M (p<0.05). In isolated rabbit hearts, Adrenochrome possesses deleterious effects on MI only at a very high concentration but not in a micromolar concentration. Therefore, it seems that aminochromes may be less cardiotoxic than catecholamines.

Alsu R. Mukhametshina - One of the best experts on this subject based on the ideXlab platform.

  • Effect of silica coating and further silica surface decoration by phospholipid bilayer on quenching of Tb(III) complexes by Adrenochrome
    Journal of Molecular Liquids, 2015
    Co-Authors: Alsu R. Mukhametshina, Asiya R. Mustafina, Rustem Amirov, Konstantin A. Petrov, Victor V. Syakaev, Alexander I Konovalov
    Abstract:

    Abstract The present report introduces regularities and mechanisms of Tb(III)-centered luminescence quenching by Adrenochrome for Tb(III)-p-sulfonatothiacalix[4]arene complexes in the aqueous solutions and the same complexes doped into silica nanoparticles. The choice of Adrenochrome (the oxidized form of adrenaline) as quencher originates from its quenching effect on the Tb(III)-centered luminescence, which discriminates it from adrenaline and dopamine. The quenching through dynamic mechanism of the Tb(III) complexes in the solutions results from their concentration induced collision with Adrenochrome molecules. The quenching of the Tb(III)-doped silica nanoparticles also occurs through dynamic mechanism, although it is insignificant due to the shielding effect of the silica surface. The inclusion of the Tb(III)-doped silica nanoparticles into phospholipid bilayers influences the quenching of the Tb(III)-centered luminescence by Adrenochrome due to its binding with the bilayers deposited onto silica nanoparticles.

A. F. E. Rump - One of the best experts on this subject based on the ideXlab platform.

  • Studies on the role of superoxide anion radicals for the cardiotoxicity of Adrenochrome.
    Drug Research, 2011
    Co-Authors: A. F. E. Rump, Kuno Güttler, R Rosen, Jörg Michael Schierholz, W. Klaus
    Abstract:

    Adrenochrome is an oxidative product of adrenaline and possesses cardiotoxic properties. As oxygen free radicals play a role in the cytotoxic effects of catecholamines, the role of superoxide anion radicals, as mediators of Adrenochrome toxicity, was investigated using electrically-driven Langendorff rabbit hearts with depleted catecholamine stores. Repetitive regional myocardial ischemia (MI) was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH-fluorescence photography. Adrenochrome (10 −4 mol/l) was added to the perfusion solution after a reperfusion period of 20 min, 30 min before the 2nd coronary occlusion, with or without the additional application of SOD (30 U/ml). Left ventricular pressure was significantly enhanced by Adrenochrome (p

  • Studies on the role of superoxide anion radicals for the cardiotoxicity of Adrenochrome.
    Arzneimittel-Forschung, 2011
    Co-Authors: A. F. E. Rump, Kuno Güttler, R Rosen, Jörg Michael Schierholz, W. Klaus
    Abstract:

    Adrenochrome is an oxidative product of adrenaline and possesses cardiotoxic properties. As oxygen free radicals play a role in the cytotoxic effects of catecholamines, the role of superoxide anion radicals, as mediators of Adrenochrome toxicity, was investigated using electrically-driven Langendorff rabbit hearts with depleted catecholamine stores. Repetitive regional myocardial ischemia (MI) was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH-fluorescence photography. Adrenochrome (10(-6) mol/l) was added to the perfusion solution after a reperfusion period of 20 min, 30 min before the 2nd coronary occlusion, with or without the additional application of SOD (30 U/ml). Left ventricular pressure was significantly enhanced by Adrenochrome (p < 0.05), but it fell rapidly down below its initial value (p < 0.05). Coronary flow was significantly decreased by Adrenochrome (p < 0.05). Whereas epicardial NADH-fluorescence was similar after repetitive coronary occlusions in untreated controls, it was significantly enhanced by Adrenochrome (p < 0.05). The deleterious effects of Adrenochrome on MI were not inhibited by SOD. Thus, there is no evidence for superoxide anion radicals as mediators of the deleterious effects of Adrenochrome on MI in isolated rabbit hearts. The deleterious effects of Adrenochrome on MI in isolated rabbit hearts might be caused by functional effects, impairing the oxygen consumption/oxygen supply balance.

  • Functional Effects of Adrenochrome in Isolated Rabbit Heart
    Pharmacology & Toxicology, 1995
    Co-Authors: A. F. E. Rump, W. Klaus
    Abstract:

    : The cardiotoxic effects of catecholamines have been explained in part by the generation of oxygen free radicals and aminochromes. The role of aminochromes remains however controversial. It has previously been demonstrated that Adrenochrome, an oxidation product of adrenaline, shows cardiotoxic properties only at very high concentrations, and it has been suggested that the deleterious effects observed may be caused by a worsening in myocardial perfusion. The functional properties of Adrenochrome were examined in isolated spontaneously-beating rabbit hearts with depleted catecholamine stores (reserpin 7.0 mg/kg 16-24 hr before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, [Ca++]sol. 1.8 mmol/l, 37 degrees). Cumulative concentration-response curves show an Adrenochrome-concentration-dependent increase of contractility (left ventricular pressure, EC50 = 3.6 x 10(-6) M; +dp/dtmax, EC50 = 1.6 x 10(-5) M), whereas myocardial relaxation was impaired (-dp/dtmax, EC50 = 2.6 x 10(-5) M; -dp/dtmax/+dp/dtmax = 0.68 at 10(-4) M). Heart-rate was only slightly enhanced (+10% at 10(-4) M), and the coronary flow was markedly influenced only by Adrenochrome 10(-4) M (-17%). The relative coronary flow (= global coronary flow/pressure-rate product) was concentration-dependently reduced (EC50 = 10(-5) M; -49% at 10(-4) M). We conclude that in isolated rabbit hearts, Adrenochrome has a positive inotropic action but impairs myocardial relaxation, and coronary constrictor activity prevents an increase of myocardial oxygen supply, thus worsening myocardial oxygen-demand/supply balance.

  • Cardiotoxicity of Adrenochrome in isolated rabbit hearts assessed by epicardial NADH fluorescence.
    Archives of Toxicology, 1994
    Co-Authors: A. F. E. Rump, W. Klaus
    Abstract:

    Noradrenaline in a micromolar concentration has recently been shown to contribute to ischemic tissue injury by direct cardiotoxic effects independent of functional alterations. Oxygen free radicals, generated during the auto-oxidation of catecholamines, are important mediators of catecholamine cardiotoxicity. However, the role of the oxidative products (aminochromes) is still unclear. We examined the effects of Adrenochrome on functional parameters and on regional myocardial ischemia (MI) in isolated electrically-driven rabbit hearts with depleted catecholamine stores (reserpine 7.0 mg/kg i.p. 16–24 h before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37°C). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH fluorescence photography. Adrenochrome-treatment (10−6 M or 10−4 M) was started after a reperfusion period of 20 min. The left ventricular pressure (LVP) was significantly enhanced by Adrenochrome (p 0.05), but it was significantly decreased by Adrenochrome 10−4 M (P 0.05) and more markedly by Adrenochrome 10−4 M (p 0.05), it was significantly enhanced by Adrenochrome 10−4 M (p

  • cardiotoxicity of Adrenochrome in isolated rabbit hearts assessed by epicardial nadh fluorescence
    Archives of Toxicology, 1994
    Co-Authors: A. F. E. Rump, W. Klaus
    Abstract:

    Noradrenaline in a micromolar concentration has recently been shown to contribute to ischemic tissue injury by direct cardiotoxic effects independent of functional alterations. Oxygen free radicals, generated during the auto-oxidation of catecholamines, are important mediators of catecholamine cardiotoxicity. However, the role of the oxidative products (aminochromes) is still unclear. We examined the effects of Adrenochrome on functional parameters and on regional myocardial ischemia (MI) in isolated electrically-driven rabbit hearts with depleted catecholamine stores (reserpine 7.0 mg/kg i.p. 16–24 h before preparation, Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca++ 1.8 mmol/l, 37°C). Repetitive MI, separated by a reperfusion period of 50 min, was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH fluorescence photography. Adrenochrome-treatment (10−6 M or 10−4 M) was started after a reperfusion period of 20 min. The left ventricular pressure (LVP) was significantly enhanced by Adrenochrome (p 0.05), but it was significantly decreased by Adrenochrome 10−4 M (P 0.05) and more markedly by Adrenochrome 10−4 M (p 0.05), it was significantly enhanced by Adrenochrome 10−4 M (p<0.05). In isolated rabbit hearts, Adrenochrome possesses deleterious effects on MI only at a very high concentration but not in a micromolar concentration. Therefore, it seems that aminochromes may be less cardiotoxic than catecholamines.

Rustem Amirov - One of the best experts on this subject based on the ideXlab platform.

  • Effect of silica coating and further silica surface decoration by phospholipid bilayer on quenching of Tb(III) complexes by Adrenochrome
    Journal of Molecular Liquids, 2015
    Co-Authors: Alsu R. Mukhametshina, Asiya R. Mustafina, Rustem Amirov, Konstantin A. Petrov, Victor V. Syakaev, Alexander I Konovalov
    Abstract:

    Abstract The present report introduces regularities and mechanisms of Tb(III)-centered luminescence quenching by Adrenochrome for Tb(III)-p-sulfonatothiacalix[4]arene complexes in the aqueous solutions and the same complexes doped into silica nanoparticles. The choice of Adrenochrome (the oxidized form of adrenaline) as quencher originates from its quenching effect on the Tb(III)-centered luminescence, which discriminates it from adrenaline and dopamine. The quenching through dynamic mechanism of the Tb(III) complexes in the solutions results from their concentration induced collision with Adrenochrome molecules. The quenching of the Tb(III)-doped silica nanoparticles also occurs through dynamic mechanism, although it is insignificant due to the shielding effect of the silica surface. The inclusion of the Tb(III)-doped silica nanoparticles into phospholipid bilayers influences the quenching of the Tb(III)-centered luminescence by Adrenochrome due to its binding with the bilayers deposited onto silica nanoparticles.