An endogenous dopaminergic neurotoxin: Implication for Parkinson's disease
References (37)
- et al.
Identification of catecholamine-derived alkaloids in mammals by chromatography and mass spectrometry
J Chromatography
(1974) - et al.
Release, storage, and uptake of catecholamines by a clonal cell line of nerve growth factor (NGF) responsive pheochromocytoma cells
Brain Res
(1977) Aging and neurotoxins as causative factors in idiopathic Parkinson's disease—a critical analysis of the neurochemical evidence
Prog Neuropsychopharmacol Biol Psychiatry
(1989)- et al.
Glutathione peroxidase activity in Parkinson's disease brain
Neurosci Lett
(1985) - et al.
Conformation of a dopamine metabolite in Parkinsonian brain tissue by gas chromatography/mass spectrometry
J Chromatography. Biomedical Application
(1993) - et al.
The reaction of acetaldehyde with brain microtubular proteins: formation of stable adducts and inhibition of polymerization
Neurosci Lett
(1987) - et al.
Effect of 1-methyl-4-phenylpyridinium ion (MPP+) on cathecholamine levels and activity of related enzymes in clonal rat pheochromocytoma PC12 cells
Life Sci
(1988) - et al.
Parkinson's disease: a disorder due to nigral glutathione deficiency
Neurosci Lett
(1982) - et al.
Energy-driven uptake of N-methyl-4-phenylpyridine by brain mitochondria mediates the toxicity of MPTP
Life Sci
(1986) - et al.
Specific lysis by 6-hydroxydopamine of catecholaminergic synaptosomes prepared from rat cerebrum
Brain Res
(1984)
The role of environmental toxins in the etiology of Parkinson's disease
Trends Neurosci
(1989)
Transmitter synthesis increase in substantia nigra neurons of the aged mouse
Neurosci Lett
(1991)
Compensatory mechanism in degenerative neurological diseases
Insight from parkinsonism
Arch Neurol
(1991)
The endogenous toxin hypothesis of the etiology of Parkinson's disease and a pilot trial of high-dosage antioxidant in an attempt to slow the progression of the illness
Ann NY Acad Sci
(1989)
The oxidant stress hypothesis in Parkinson's disease: evidence supporting it
Ann Neurol
(1992)
Ageing and Parkinson's disease: substantia nigra regional selectivity
Brain
(1991)
Optimum reaction conditions for human lactate dehydrogenase isoenzymes as they affect total lactate dehydrogenase activity
Clin Chem
(1968)
Establishment of a nonadrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor
Cited by (89)
Superoxide is the critical driver of DOPAL autoxidation, lysyl adduct formation, and crosslinking of α-synuclein
2017, Biochemical and Biophysical Research CommunicationsCitation Excerpt :This peculiar property suggests that oxidation of the DOPAL catechol group to a semiquinone (loss of a single electron) or quinone (loss of two electrons) activates its aldehyde's reactivity [9,10]. The catecholaldehyde hypothesis is supported by the fact that DOPAL is highly toxic in vivo and in cultured neurons and leads to the loss of dopaminergic neurons when injected into the substantia nigra of rats [11–13]. DOPAL's neuronal toxicity is accompanied by the accumulation of oligomeric forms of α-synuclein, and DOPAL also potently crosslinks α-synuclein in vitro [13–15].
Copyright © 1995 Published by Elsevier Ltd.