Taurine inhibition of metal-stimulated catecholamine oxidation

2000 ◽  
Vol 2 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Ralph Dawson ◽  
Deron Baker ◽  
Baerbel Eppler ◽  
Elisa Tang ◽  
Debbie Shih ◽  
...  
Keyword(s):  
Catecholamine Oxidation

Taurine Inhibition of Iron-Stimulated Catecholamine Oxidation

1998 ◽  
pp. 155-162 ◽  
Author(s):  
Ralph Dawson ◽  
Elisa Tang ◽  
Debbie Shih ◽  
Hunter Hern ◽  
Ming Hu ◽  
...  
Keyword(s):  
Catecholamine Oxidation

scholarly journals Melanin Biosynthesis in Cryptococcus neoformans

1998 ◽  
Vol 180 (6) ◽  
pp. 1570-1572 ◽  
Author(s):  
Peter R. Williamson ◽  
Kazumasa Wakamatsu ◽  
Shosuke Ito
Keyword(s):  
Hydrogen Peroxide ◽  
Cryptococcus Neoformans ◽  
Oxidative Coupling ◽  
Hydriodic Acid ◽  
Peroxide Oxidation ◽  
Alkaline Hydrogen Peroxide ◽  
Melanin Biosynthesis ◽  
Permanganate Oxidation ◽  
Catecholamine Oxidation ◽  
Chemical Evidence

ABSTRACT Pigment production by Cryptococcus neoformans is virulence associated. Dopamine- and 3,4-dihydroxyphenylalanine–melanin products were identified after acidic permanganate oxidation, alkaline hydrogen peroxide oxidation, or hydrolysis with hydriodic acid. These data provide direct chemical evidence for the formation of eumelanin polymers by catecholamine oxidation by laccase alone followed by oxidative coupling of dihydroxyindole.

Inhibition of catecholamine oxidation by indoles

1972 ◽  
Vol 21 (15) ◽  
pp. 2007-2012 ◽  
Author(s):  
R. Hartley ◽  
J.A. Smith
Keyword(s):  
Catecholamine Oxidation

scholarly journals Influence of the supramolecular arrangement of iron phthalocyanine thin films on catecholamine oxidation

2019 ◽  
Vol 836 ◽  
pp. 7-15 ◽  
Author(s):  
Cibely S. Martin ◽  
Priscila Alessio ◽  
Frank N. Crespilho ◽  
Christopher M.A. Brett ◽  
Carlos J.L. Constantino
Keyword(s):  
Thin Films ◽  
Iron Phthalocyanine ◽  
Catecholamine Oxidation

Role of catecholamine oxidation in sudden cardiac death

2010 ◽  
Vol 24 (5) ◽  
pp. 539-546 ◽  
Author(s):  
Naranjan S. Dhalla ◽  
Adriana Adameova ◽  
Meera Kaur
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Catecholamine Oxidation

Noradrenergic turnover increases in locus coeruleus after hemorrhage in cats

1988 ◽  
Vol 254 (2) ◽  
pp. R296-R301
Author(s):  
K. V. Thrivikraman ◽  
D. E. Carlson ◽  
D. S. Gann
Keyword(s):  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Locus Coeruleus ◽  
High Performance ◽  
In Vivo Voltammetry ◽  
Oxidation Current ◽  
Alpha Chloralose ◽  
Catecholamine Oxidation ◽  
Acth Release

Push-pull perfusion was used to determine monoaminergic activity in the locus coeruleus (LC) of alpha-chloralose-urethan-anesthetized cats after 20% hemorrhage. Blood was withdrawn from 0 to 3 min and reinfused from 10 to 13 min. Continuous 5-min interval samples of perfusate were collected from -5 to 15 min. Concentrations of the monoamines were determined using high-performance liquid chromatography with electrochemical detection. The perfusion sites (n = 21) were identified histologically. In a group of eight contiguous sites in the ventral LC (vLC), 4-hydroxy-3-methoxy-phenyl(ethylene)glycol (MHPG) increased significantly from 0.50 +/- 0.22 (control) to 1.19 +/- 0.42 pmol/5 min during the first 5 min after hemorrhage (P less than 0.05). This response differed significantly from that obtained at the remaining 13 sites. Other metabolites were not often detectable for many sites either within or outside vLC, and their responses to hemorrhage were not significant. The response of MHPG in the vLC indicates that norepinephrine (NE) turnover increases in this area selectively and implicates NE in the increase in the catecholamine oxidation current reported previously using in vivo voltammetry. Since the vLC was shown previously to facilitate adrenocorticotropin (ACTH) release, the increase in NE turnover after hemorrhage could induce ACTH release. This increase may also act locally to modulate the ascending hemodynamic signal.

scholarly journals An Unrecognized Fundamental Relationship between Neurotransmitters: Glutamate Protects against Catecholamine Oxidation

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1564
Author(s):  
Wenping Wang ◽  
Ximing Wu ◽  
Chung S. Yang ◽  
Jinsong Zhang
Keyword(s):  
Dna Damage ◽  
Neurodegenerative Diseases ◽  
Hydroxyl Radicals ◽  
Redox Activity ◽  
Molar Ratio ◽  
Protective Mechanism ◽  
Effective Prevention ◽  
Excitatory Neurotransmitter ◽  
Catecholamine Oxidation

Neurotransmitter catecholamines (dopamine, epinephrine, and norepinephrine) are liable to undergo oxidation, which copper is deeply involved in. Catecholamine oxidation-derived neurotoxicity is recognized as a pivotal pathological mechanism in neurodegenerative diseases. Glutamate, as an excitatory neurotransmitter, is enriched in the brain at extremely high concentrations. However, the chemical biology relationship of these two classes of neurotransmitters remains largely unknown. In the present study, we assessed the influences of glutamate on the autoxidation of catecholamines, the copper- and copper-containing ceruloplasmin-mediated oxidation of catecholamines, the catecholamine-induced formation of quinoprotein, catecholamine/copper-induced hydroxyl radicals, and DNA damage in vitro. The results demonstrate that glutamate, at a physiologically achievable molar ratio of glutamate/catecholamines, has a pronounced inhibitory effect on catecholamine oxidation, catecholamine oxidation-evoked hydroxyl radicals, quinoprotein, and DNA damage. The protective mechanism of glutamate against catecholamine oxidation could be attributed to its restriction of the redox activity of copper via chelation. This previously unrecognized link between glutamate, catecholamines, and copper suggests that neurodegenerative disorders may occur and develop once the built-in equilibrium is disrupted and brings new insight into developing more effective prevention and treatment strategies for neurodegenerative diseases.

Ascorbic acid as an antioxidant in measurements of catecholamines in plasma.

1987 ◽  
Vol 33 (4) ◽  
pp. 569-571 ◽  
Author(s):  
D Hugh ◽  
A Grennan ◽  
M A Abugila ◽  
C Weinkove
Keyword(s):  
Ascorbic Acid ◽  
Acetic Acid ◽  
Atmospheric Oxygen ◽  
Electrochemical Measurement ◽  
Sodium Metabisulfite ◽  
Subsequent Degradation ◽  
Catecholamine Oxidation

Abstract Sodium metabisulfite, commonly used to prevent the oxidation of catecholamines during extraction from plasma onto alkaline alumina, does not prevent their subsequent degradation in acetic acid eluates. However, ascorbic acid, a potent antioxidant, is extracted with the catecholamines onto the alumina and prevents such destruction. However, ascorbic acid may interfere with the electrochemical measurement of catecholamines, unless sequential oxidation and reduction are used. Other methods of minimizing catecholamine oxidation in acetic acid eluates include refrigerating at 4 degrees C and capping the sample vials to exclude atmospheric oxygen.

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