39984-17-3

Basic information

• Product Name: aminochrome 1
• Synonyms: aminochrome 1
• CAS NO: 39984-17-3
• Molecular Formula: C₈H₇NO₂
• Molecular Weight: 149.15
• Mol File: 39984-17-3.mol
• Article Data: 5

Chemical Properties

• Boiling Point: 323.7°Cat760mmHg
• Flash Point: 160.1°C
• Appearance: /
• Density: 1.33g/cm³
• Vapor Pressure: 0.000258mmHg at 25°C
• Refractive Index: 1.599
• CAS DataBase Reference: aminochrome 1(CAS DataBase Reference)
• NIST Chemistry Reference: aminochrome 1(39984-17-3)
• EPA Substance Registry System: aminochrome 1(39984-17-3)

Safety Data

• Hazardous Substances Data: 39984-17-3(Hazardous Substances Data)

Usage

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 articles and documents

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.).

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

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.