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Journal ArticleDOI

Toxic effects of L-DOPA on mesencephalic cell cultures: protection with antioxidants

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TLDR
The damage of DA neurons took place before the rising of quinones, suggesting thatQuinones are not essential in L-DOPA toxicity for DA neurons, and antioxidants completely prevented L- DOPA-induced quinone formation as well as the death of non-DA neurons.
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This article is published in Brain Research.The article was published on 1995-06-05. It has received 145 citations till now. The article focuses on the topics: Neurotoxicity & Ascorbic acid.

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Functional changes of the basal ganglia circuitry in Parkinson's disease.

TL;DR: The identification of the role of the subthalamic nucleus and, more in general, of the glutamatergic mechanisms in the pathophysiology of Parkinson's disease might lead to a new approach in the pharmacological treatment of the disease.
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Parkin gene inactivation alters behaviour and dopamine neurotransmission in the mouse

TL;DR: It is shown that inactivation of the parkin gene in mice results in motor and cognitive deficits, inhibition of amphetamine-induced dopamine release and inhibition of glutamate neurotransmission, and the levels of dopamine are increased in the limbic brain areas of parkin mutant mice and there is a shift towards increased metabolism of dopamine by MAO.
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Interplay between Cytosolic Dopamine, Calcium, and α-Synuclein Causes Selective Death of Substantia Nigra Neurons

TL;DR: Using intracellular patch electrochemistry to directly measure cytosolic dopamine in cultured midbrain neurons, it is confirmed that elevated DA(cyt) and its metabolites are neurotoxic and that genetic and pharmacological interventions that decrease DA(Cyt) provide neuroprotection.
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Dopamine- or L-DOPA-induced neurotoxicity: the role of dopamine quinone formation and tyrosinase in a model of Parkinson's disease.

TL;DR: The double-edged synthesizing and oxidizing functions of tyrosinase in the dopaminergic system suggest its potential for application in the synthesis of DA, instead of TH in the degeneration of dopamine neurons, and in the normalization of abnormal DA turnover in long-term L-DOPA-treated Parkinson's disease patients.
References
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A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

TL;DR: This assay is very reproducible and rapid with the dye binding process virtually complete in approximately 2 min with good color stability for 1 hr with little or no interference from cations such as sodium or potassium nor from carbohydrates such as sucrose.
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Basal Lipid Peroxidation in Substantia Nigra Is Increased in Parkinson's Disease

TL;DR: The results may indicate that an increased level of lipid peroxidation continues to occur in the parkinsonian nigra up to the time of death, perhaps because of continued exposure to excess free radicals derived from some endogenous or exogenous neurotoxic species.
Journal Article

Oxidative Pathways for Catecholamines in the Genesis of Neuromelanin and Cytotoxic Quinones

TL;DR: The autoxidation, periodate oxidation, and tyrosinase-mediated oxidation of 6-hydroxydopamine, dopamine, norepinephrine, and epinephrine were studied by absorption spectroscopy and gave evidence for a transient intermediate, the o -quinone, which rapidly tautomerized to the p-quinone.
Journal Article

Autoxidation versus covalent binding of quinones as the mechanism of toxicity of dopamine, 6-hydroxydopamine, and related compounds toward C1300 neuroblastoma cells in vitro

TL;DR: 6-hydroxydopamine and 2,4,5-trihydroxyphenylalanine kill cells through the production of H2O2, O2[unknown], and OH·, while for dopamine and dopa the reaction of quinone oxidation products with nucleophiles probably also contributes to their cytotoxicity.
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