3-O-Methyldopa - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

3-O-Methyldopa

The Experts below are selected from a list of 165 Experts worldwide ranked by ideXlab platform

3-O-Methyldopa – Free Register to Access Experts & Abstracts

Yvette Michotte – One of the best experts on this subject based on the ideXlab platform.

  • In vivo pharmacokinetics of levodopa and 3-O-Methyldopa in muscle
    Naunyn-Schmiedeberg's Archives of Pharmacology, 1992
    Co-Authors: Dirk Deleu, Sophie Sarre, Guy Ebinger, Yvette Michotte
    Abstract:

    In the present study in vivo microdialysis sampling coupled to high-performance liquid chrochromatography with electrochemical detection, was used to study the pharmacokinetics of levodopa and 3-O-Methyldopa in skeletal muscle in dog, after intravenous administration of levodopa. For comparison, the pharmacokinetic parameters of both compounds were simultaneously determined in plasma using blood collection. Muscle microdialysis samples and blood were continuously collected for 4 h after the administration of levodopa (25 mg/kg). Pharmacokinetic profiles of levodopa in plasma and muscle were different. The mean Tmax value of levodopa in plasma and muscle was 0.16 h and 1.0 h, respectively.

  • In vivo pharmacokinetics of levodopa and 3-O-Methyldopa in muscle
    Naunyn-Schmiedeberg's Archives of Pharmacology, 1991
    Co-Authors: Dirk Deleu, Sophie Sarre, Guy Ebinger, Yvette Michotte
    Abstract:

    In the present study in vivo microdialysis sampling coupled to high-performance liquid chrochromatography with electrochemical detection, was used to study the pharmacokinetics of levodopa and 3-O-Methyldopa in skeletal muscle in dog, after intravenous administration of levodopa. For comparison, the pharmacokinetic parameters of both compounds were simultaneously determined in plasma using blood collection. Muscle microdialysis samples and blood were continuously collected for 4 h after the administration of levodopa (25 mg/kg). Pharmacokinetic profiles of levodopa in plasma and muscle were different. The mean Tmax value of levodopa in plasma and muscle was 0.16 h and 1.0 h, respectively. The AUC_0→inf for levodopa in plasma was nearly 18-fold higher in plasma than in muscle. The 3-O-Methyldopa concentration increased very rapidly after the administration of levodopa, to reach a plateau after 2.5 h and 3 h in plasma and muscle, respectively. The AUC_0→4 for 3-O-Methyldopa was 3.6-fold higher in plasma than in muscle. The ratio levodopa/3-O-Methyldopa, reflecting the metabolic rate of levodopa, was 3.5 times higher in plasma than in muscle, at the peak value of levodopa, and then rapidly declined to values lower than 1, one hour after administration of the drug. We compared our results with literature data from postmortem studies done in rat experiments. We concluded that levodopa is not accumulating in muscle as such, but is converted to 3-O-Methyldopa probably before leaving the plasma compartment.

  • In vivo pharmacokinetics of levodopa and 3-O-Methyldopa in muscle. A microdialysis study.
    Naunyn-Schmiedeberg's archives of pharmacology, 1991
    Co-Authors: Dirk Deleu, Sophie Sarre, Guy Ebinger, Yvette Michotte
    Abstract:

    In the present study in vivo microdialysis sampling coupled to high-performance liquid chrochromatography with electrochemical detection, was used to study the pharmacokinetics of levodopa and 3-O-Methyldopa in skeletal muscle in dog, after intravenous administration of levodopa. For comparison, the pharmacokinetic parameters of both compounds were simultaneously determined in plasma using blood collection. Muscle microdialysis samples and blood were continuously collected for 4 h after the administration of levodopa (25 mg/kg). Pharmacokinetic profiles of levodopa in plasma and muscle were different. The mean Tmax value of levodopa in plasma and muscle was 0.16 h and 1.0 h, respectively. The AUC0—-inf for levodopa in plasma was nearly 18-fold higher in plasma than in muscle. The 3-O-Methyldopa concentration increased very rapidly after the administration of levodopa, to reach a plateau after 2.5 h and 3 h in plasma and muscle, respectively. The AUC0—-4 for 3-O-Methyldopa was 3.6-fold higher in plasma than in muscle. The ratio levodopa/3-O-Methyldopa, reflecting the metabolic rate of levodopa, was 3.5 times higher in plasma than in muscle, at the peak value of levodopa, and then rapidly declined to values lower than 1, one hour after administration of the drug. We compared our results with literature data from postmortem studies done in rat experiments. We concluded that levodopa is not accumulating in muscle as such, but is converted to 3-O-Methyldopa probably before leaving the plasma compartment.

Siegfried Muhlack – One of the best experts on this subject based on the ideXlab platform.

Thomas Müller – One of the best experts on this subject based on the ideXlab platform.

  • Levodopa-related cysteinyl–glycine and cysteine reduction with and without catechol-O-methyltransferase inhibition in Parkinson’s disease patients
    Journal of Neural Transmission, 2014
    Co-Authors: Thomas Müller, Siegfried Muhlack
    Abstract:

    Oxidative stress is influenced by the thiol homeostasis, which regulates the redox milieu via glutathione. Components of glutathione metabolism are cysteine and cysteinyl–glycine. Both substrates decay following levodopa application or dopamine-related oxidative stress. Objective was to investigate the impact of an acute levodopa application with and without catechol- O -methyltransferase inhibitor on cysteine- and cysteinyl–glycine plasma levels. On two investigation days, 13 patients with Parkinson’s disease took one retarded release 200-mg levodopa/50 mg carbidopa-containing tablet or one 150-mg levodopa/50-mg carbidopa/200-mg entacapone formulation under standardized conditions. Levodopa, 3- O -methyldopa, cysteine and cysteinyl–glycine were measured at baseline, 80 and 140 min following levodopa administration. Cysteine and cysteinyl–glycine similarly decreased, levodopa was nearly equal during both conditions. Entacapone lowered 3- O -methyldopa. Cysteine decay may be due to an elevated glutathione generation, which consumes cysteine. Cysteinyl–glycine decrease results from the alternative glutathione transformation to its oxidized form glutathione dissulfide after free radical scavenging.

  • fewer fluctuations higher maximum concentration and better motor response of levodopa with catechol o methyltransferase inhibition
    Journal of Neural Transmission, 2014
    Co-Authors: Siegfried Muhlack, Lennard Herrmann, Stephan Salmen, Thomas Müller
    Abstract:

    Catechol-O-methyltransferase inhibitor addition to levodopa/carbidopa formulations improves motor symptoms and reduces levodopa fluctuations in patients with Parkinson’s disease. Objectives were to investigate the effects of entacapone and tolcapone on plasma behaviour of levodopa, its metabolite 3-O-Methyldopa and on motor impairment. 22 patients orally received levodopa/carbidopa first, then levodopa/carbidopa/entacapone and finally levodopa/carbidopa plus tolcapone within a 4.5 h interval twice. Maximum concentration, time to maximum level and bioavailability of levodopa did not differ between all conditions each with 200 mg levodopa application as a whole. Catechol-O-methyltransferase inhibition caused less fluctuations and higher baseline levels of levodopa after the first intake and less 3-O-Methyldopa appearance. The maximum levodopa concentrations were higher after the second levodopa intake, particularly with catechol-O-methyltransferase inhibition. The motor response to levodopa was better with catechol-O-methyltransferase inhibition than without, tolcapone was superior to entacapone. More continuous levodopa brain delivery and lower 3-O-Methyldopa bioavailability caused a better motor response during catechol-O-methyltransferase inhibition.

  • Levodopa-related cysteinyl-glycine and cysteine reduction with and without catechol-O-methyltransferase inhibition in Parkinson’s disease patients.
    Journal of neural transmission (Vienna Austria : 1996), 2014
    Co-Authors: Thomas Müller, Siegfried Muhlack
    Abstract:

    Oxidative stress is influenced by the thiol homeostasis, which regulates the redox milieu via glutathione. Components of glutathione metabolism are cysteine and cysteinyl–glycine. Both substrates decay following levodopa application or dopamine-related oxidative stress. Objective was to investigate the impact of an acute levodopa application with and without catechol-O-methyltransferase inhibitor on cysteine- and cysteinyl–glycine plasma levels. On two investigation days, 13 patients with Parkinson’s disease took one retarded release 200-mg levodopa/50 mg carbidopa-containing tablet or one 150-mg levodopa/50-mg carbidopa/200-mg entacapone formulation under standardized conditions. Levodopa, 3-O-Methyldopa, cysteine and cysteinyl–glycine were measured at baseline, 80 and 140 min following levodopa administration. Cysteine and cysteinyl–glycine similarly decreased, levodopa was nearly equal during both conditions. Entacapone lowered 3-O-Methyldopa. Cysteine decay may be due to an elevated glutathione generation, which consumes cysteine. Cysteinyl–glycine decrease results from the alternative glutathione transformation to its oxidized form glutathione dissulfide after free radical scavenging.

Dirk Deleu – One of the best experts on this subject based on the ideXlab platform.

  • In vivo pharmacokinetics of levodopa and 3-O-Methyldopa in muscle
    Naunyn-Schmiedeberg's Archives of Pharmacology, 1992
    Co-Authors: Dirk Deleu, Sophie Sarre, Guy Ebinger, Yvette Michotte
    Abstract:

    In the present study in vivo microdialysis sampling coupled to high-performance liquid chromatography with electrochemical detection, was used to study the pharmacokinetics of levodopa and 3-O-Methyldopa in skeletal muscle in dog, after intravenous administration of levodopa. For comparison, the pharmacokinetic parameters of both compounds were simultaneously determined in plasma using blood collection. Muscle microdialysis samples and blood were continuously collected for 4 h after the administration of levodopa (25 mg/kg). Pharmacokinetic profiles of levodopa in plasma and muscle were different. The mean Tmax value of levodopa in plasma and muscle was 0.16 h and 1.0 h, respectively.

  • In vivo pharmacokinetics of levodopa and 3-O-Methyldopa in muscle
    Naunyn-Schmiedeberg's Archives of Pharmacology, 1991
    Co-Authors: Dirk Deleu, Sophie Sarre, Guy Ebinger, Yvette Michotte
    Abstract:

    In the present study in vivo microdialysis sampling coupled to high-performance liquid chromatography with electrochemical detection, was used to study the pharmacokinetics of levodopa and 3-O-Methyldopa in skeletal muscle in dog, after intravenous administration of levodopa. For comparison, the pharmacokinetic parameters of both compounds were simultaneously determined in plasma using blood collection. Muscle microdialysis samples and blood were continuously collected for 4 h after the administration of levodopa (25 mg/kg). Pharmacokinetic profiles of levodopa in plasma and muscle were different. The mean Tmax value of levodopa in plasma and muscle was 0.16 h and 1.0 h, respectively. The AUC_0→inf for levodopa in plasma was nearly 18-fold higher in plasma than in muscle. The 3-O-Methyldopa concentration increased very rapidly after the administration of levodopa, to reach a plateau after 2.5 h and 3 h in plasma and muscle, respectively. The AUC_0→4 for 3-O-Methyldopa was 3.6-fold higher in plasma than in muscle. The ratio levodopa/3-O-Methyldopa, reflecting the metabolic rate of levodopa, was 3.5 times higher in plasma than in muscle, at the peak value of levodopa, and then rapidly declined to values lower than 1, one hour after administration of the drug. We compared our results with literature data from postmortem studies done in rat experiments. We concluded that levodopa is not accumulating in muscle as such, but is converted to 3-O-Methyldopa probably before leaving the plasma compartment.

  • In vivo pharmacokinetics of levodopa and 3-O-Methyldopa in muscle. A microdialysis study.
    Naunyn-Schmiedeberg's archives of pharmacology, 1991
    Co-Authors: Dirk Deleu, Sophie Sarre, Guy Ebinger, Yvette Michotte
    Abstract:

    In the present study in vivo microdialysis sampling coupled to high-performance liquid chromatography with electrochemical detection, was used to study the pharmacokinetics of levodopa and 3-O-Methyldopa in skeletal muscle in dog, after intravenous administration of levodopa. For comparison, the pharmacokinetic parameters of both compounds were simultaneously determined in plasma using blood collection. Muscle microdialysis samples and blood were continuously collected for 4 h after the administration of levodopa (25 mg/kg). Pharmacokinetic profiles of levodopa in plasma and muscle were different. The mean Tmax value of levodopa in plasma and muscle was 0.16 h and 1.0 h, respectively. The AUC0—-inf for levodopa in plasma was nearly 18-fold higher in plasma than in muscle. The 3-O-Methyldopa concentration increased very rapidly after the administration of levodopa, to reach a plateau after 2.5 h and 3 h in plasma and muscle, respectively. The AUC0—-4 for 3-O-Methyldopa was 3.6-fold higher in plasma than in muscle. The ratio levodopa/3-O-Methyldopa, reflecting the metabolic rate of levodopa, was 3.5 times higher in plasma than in muscle, at the peak value of levodopa, and then rapidly declined to values lower than 1, one hour after administration of the drug. We compared our results with literature data from postmortem studies done in rat experiments. We concluded that levodopa is not accumulating in muscle as such, but is converted to 3-O-Methyldopa probably before leaving the plasma compartment.

Ikuko Miyazaki – One of the best experts on this subject based on the ideXlab platform.