39984-17-3

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InChI:InChI=1/C8H7NO2/c10-7-3-5-1-2-9-6(5)4-8(7)11/h3-4,9H,1-2H2

Upstream product

• 51-61-6 dopamine 
• 62-31-7 dopamine hydrochloride 

Relevant academic research and scientific papers

Dopamine promotes the neurodegenerative potential of β-synuclein

A contribution of α-Synuclein (α-Syn) to etiology of Parkinson′s disease (PD) and Dementia with Lewy bodies (DLB) is currently undisputed, while the impact of the closely related β-Synuclein (β-Syn) on these disorders remains enigmatic. β-Syn has long been considered to be an attenuator of the neurotoxic effects of α-Syn, but in a rodent model of PD β-Syn induced robust neurodegeneration in dopaminergic neurons of the substantia nigra. Given that dopaminergic nigral neurons are selectively vulnerable to neurodegeneration in PD, we now investigated if dopamine can promote the neurodegenerative potential of β-Syn. We show that in cultured rodent and human neurons a dopaminergic neurotransmitter phenotype substantially enhanced β-Syn-induced neurodegeneration, irrespective if dopamine is synthesized within neurons or up-taken from extracellular space. Nuclear magnetic resonance interaction and thioflavin-T incorporation studies demonstrated that dopamine and its oxidized metabolites 3,4-dihydroxyphenylacetaldehyde (DOPAL) and dopaminochrome (DCH) directly interact with β-Syn, thereby enabling structural and functional modifications. Interaction of DCH with β-Syn inhibits its aggregation, which might result in increased levels of neurotoxic oligomeric β-Syn. Since protection of outer mitochondrial membrane integrity prevented the additive neurodegenerative effect of dopamine and β-Syn, such oligomers might act at a mitochondrial level similar to what is suggested for α-Syn. In conclusion, our results suggest that β-Syn can play a significant pathophysiological role in etiology of PD through its interaction with dopamine metabolites and thus should be re-considered as a disease-relevant factor, at least for those symptoms of PD that depend on degeneration of nigral dopaminergic neurons. (Figure presented.).

Anaerobic oxidation of dopamine by iron(III)

Iron(III) [in the form of Fe(OH)2+] reacted reversibly in acid aqueous solution with dopamine, 2-(3,4-dihydroxyphenyl)ethylamine (H2LH+, in which the phenolic protons are written to the left of L) to give the complex ion Fe(LH)2+. This species then decomposed to yield iron(II) and a semiquinone, which in turn is oxidised further to a quinone. The latter cyclised to form leucodopaminochrome (indoline-5,6-diol), which was finally oxidised by iron(III) to pink dopaminochrome (6-hydroxy-3H-indol-5-one), presumably via another semiquinone. The rate of appearance and disappearance of the complex and of the ortho-quinone were separately followed by stopped-flow photometric methods. Mechanisms are proposed for the various steps and these are supported by measurements at varying ionic strengths. Rate constants for the reversible formation of the iron-dopamine complex have been evaluated [k1 = (2.09 ± 0.05) × 103 and k-1 = 23 ± 2 dm3 mol-1 s-1]. The rate of decomposition of the protonated complex to yield iron(II) and the semiquinone was established as k2 = 0.23 ± 0.02 s-1 and KMH = 33 ± 0.9 dm3 mol-1 [for the protonation of Fe(LH)2+]. The stability constant of the Fe(LH)2+ complex has been calculated (log K1M = 21.14) and εmax is 1260 dm3 mol-1 cm-1 at 700 nm. The effect of chloride on the rate of complex formation at low pH has been explained by the fact that FeCl2+ also reacts with dopamine (kCl = 148 ± 7 dm3 mol-1 s-1) to form the complex but that this is predominantly reversible via the non-chloride route at low pH values. The stability constant for FeCl2+ formation (a constant not readily accessible by standard methods) was extracted from the data (log K1Cl = 1.53). The rate of disappearance of the quinone enabled the ring-closure reaction (i.e. the formation of the indole) to be followed and the mechanism established. All measurements were carried out at 25°C in solutions of ionic strength 0.10 mol dm-3 (KNO3) except for ionic strength dependence studies.

Iron-mediated generation of the neurotoxin 6-hydroxydopamine quinone by reaction of fatty acid hydroperoxides with dopamine: A possible contributory mechanism for neuronal degeneration in parkinson's disease

Exposure of dopamine to an excess of linoleic acid 13-hydroperoxide (13- hydroperoxyoetadecadienoic acid) in the presence of ferrous ions in Tris buffer, pH 7.4, resulted in a relatively fast, oxygen-independent reaction exhibiting first-order kinetics wi

Spontaneous Autooxidation of Dopamine

A detailed kinetic study has been carried out of the reaction of dopamine, 2-(3,4-dihydroxyphenyl)ethylamine, with dioxygen over the pH range 7-9 where it reacts spontaneously without the necessity of metal ion catalysis.The reaction was found to be accurately first-order in and in and first-order in +>-1 and, furthermore, stoichiometric amounts of H2O2 were shown to be produced.The other product of oxidation is, initially, the pink dopaminochrome which, however, is not stable and reacts further (without the consumption of dioxygen) to form the insoluble polymeric material known as 'melanine'.The rate-determining step is assumed to be hydrogen atom abstraction from the monodeprotonated species by O2 (as with many other catecholamines, dopamine is stable towards oxidation in acidic media in the complete absence of metal ions) with a second-order rate constant of k1=0.47+/-0.05 dm3 mol-1 s-1 at 25 deg C in a solution of ionic strength 0.1 mol-1 dm-3 (KCl).

MUSHROOM TYROSINASE AS AN OXIDANT FOR THE SYNTHESIS OF 5,6-DIHYDROXYINDOLE DERIVATIVES

Several catecholamines have been converted to 5,6-diacetoxyindole derivatives by the use of mushroom tyrosinase as oxidant.