Cited by 1,126melanin and skin pigmentationParkinson's Disease Mechanisms and TreatmentsBioactive Compounds and Antitumor Agents

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

GRAHAM, DOYLE G.·1978·Molecular Pharmacology

DOI 10.1016/s0026-895x(25)13535-9

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Background
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Michel, P. P., & Hefti, F. F. (1990) · Journal of Neuroscience Research · doi:10.1002/jnr.490260405 · Cited by 339
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Background
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Background
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Influential
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The relationship between oxidative/nitrative stress and pathological inclusions in Alzheimer’s and Parkinson’s diseases1,2 11Guest Editors: Mark A. Smith and George Perry 22This article is part of a series of reviews on “Causes and Consequences of Oxidative Stress in Alzheimer’s Disease.” The full list of papers may be found on the homepage of the journal.
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Background
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Background
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Mytilineou, C., Han, S., & Cohen, G. (1993) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1993.tb13642.x · Cited by 244
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Monte, D. A. D., Lavasani, M., & Manning-Bog, A. (2002) · NeuroToxicology · doi:10.1016/s0161-813x(02)00099-2 · Cited by 244
Unregulated Cytosolic Dopamine Causes Neurodegeneration Associated with Oxidative Stress in Mice
Chen, L., Ding, Y., Cagniard, B., Laar, A. D. V., Mortimer, A. D., Chi, W., Hastings, T. G., Kang, U. J., & Zhuang, X. (2008) · Journal of Neuroscience · doi:10.1523/jneurosci.3602-07.2008 · Cited by 242
“Dopamine is a very reactive molecule compared with other neurotransmitters, and dopamine degradation naturally produces oxidative species (Graham, 1978).”
Background
Dopamine, 6-hydroxydopamine, iron, and dioxygen — their mutual interactions and possible implication in the development of Parkinson's disease
Linert, W., Herlinger, E., Jameson, R. F., Kienzl, E., Jellinger, K. A., & Youdim, M. B. H. (1996) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/0925-4439(96)00020-8 · Cited by 238
Manganese ethylene‐bis‐dithiocarbamate and selective dopaminergic neurodegeneration in rat: a link through mitochondrial dysfunction
Zhang, J., Fitsanakis, V. A., Gu, G., Jing, D., Ao, M., Amarnath, V., & Montine, T. J. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.01525.x · Cited by 238
Alpha-synuclein, lipids and Parkinson’s disease
Ruipérez, V., Darios, F. D., & Davletov, B. A. (2010) · Progress in Lipid Research · doi:10.1016/j.plipres.2010.05.004 · Cited by 236
Manganese poisoning and the attack of trivalent manganese upon catecholamines
Archibald, F. S., & Tyree, C. M. (1987) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(87)90621-7 · Cited by 231
Chronic levodopa is not toxic for remaining dopamine neurons, but instead promotes their recovery, in rats with moderate nigrostriatal lesions
Murer, M. G., Dziewczapolski, G., Menalled, L., et al. (1998) · Annals of Neurology · doi:10.1002/ana.410430504 · Cited by 232
Levodopa in the treatment of Parkinson's disease
Schapira, A. H. V., Emre, M., Jenner, P., & Poewe, W. (2009) · European Journal of Neurology · doi:10.1111/j.1468-1331.2009.02697.x · Cited by 231
Is the Vulnerability of Neurons in the Substantia Nigra of Patients with Parkinson's Disease Related to Their Neuromelanin Content?
Kästner, A., Hirsch, É. C., Lejeune, O., Javoy-Agid, F., Rascol, O., & Agid, Y. (1992) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1992.tb08350.x · Cited by 228
Neuroprotective effects of anthocyanin- and proanthocyanidin-rich extracts in cellular models of Parkinson׳s disease
Strathearn, K. E., Yousef, G. G., Grace, M. H., Roy, S. L., Tambe, M. A., Ferruzzi, M. G., Wu, Q.-L., Simon, J. E., Lila, M. A., & Rochet, J. (2014) · Brain Research · doi:10.1016/j.brainres.2014.01.047 · Cited by 231
“Dopaminergic neurons of the SNpc contain relatively high basal levels of ROS resulting from the metabolism and auto-oxidation of dopamine (Betarbet et al., 2000; Graham, 1978).”
Background
Spontaneous autoxidation of dopamine
Herlinger, E., Jameson, R. F., & Linert, W. (1995) · Journal of the Chemical Society Perkin Transactions 2 · doi:10.1039/p29950000259 · Cited by 233
Oxygen Radicals and Neuropsychiatric Illness
Lohr, J. B. (1991) · Archives of General Psychiatry · doi:10.1001/archpsyc.1991.01810360061009 · Cited by 225
Neurotoxicity of methamphetamine: Main effects and mechanisms
Jayanthi, S., Daiwile, A. P., & Cadet, J. L. (2021) · Experimental Neurology · doi:10.1016/j.expneurol.2021.113795 · Cited by 238
Mitochondria and Brain Disease: A Comprehensive Review of Pathological Mechanisms and Therapeutic Opportunities
Clemente‐Suárez, V. J., Redondo-Flórez, L., Beltrán-Velasco, A. I., Ramos‐Campo, D. J., Belinchón-deMiguel, P., Martínez‐Guardado, I., Dalamitros, A. A., Sepulveda, R. A. Y., Martín-Rodríguez, A., & Tornero-Aguilera, J. F. (2023) · Biomedicines · doi:10.3390/biomedicines11092488 · Cited by 251
Neuronal Apoptosis in Neurodegeneration
Okouchi, M., Ekshyyan, O. Y., Maracine, M., & Aw, T. Y. (2007) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.1511 · Cited by 222
“Dopamine is metabolized by monoamine oxidase which generates H 2 O 2 (225), or is autooxidized to yield O 2 (cid:2) (cid:6) radicals, H 2 O 2 , and dopamine-quinone species (116).”
Dopamine induces soluble α-synuclein oligomers and nigrostriatal degeneration
Mor, D. E., Tsika, E., Mazzulli, J. R., Gould, N. S., Kim, H., Daniels, M. J., Doshi, S., Gupta, P., Grossman, J., Tan, V. X., et al. (2017) · Nature Neuroscience · doi:10.1038/nn.4641 · Cited by 226
“At cytosolic pH, dopamine auto-oxidizes to form reactive quinone species, hydrogen peroxide, and other electrophiles (2).”
Background
Differential effects of stimulants on monoaminergic transporters: Pharmacological consequences and implications for neurotoxicity
Fleckenstein, A. E., Gibb, J. W., & Hanson, G. R. (2000) · European Journal of Pharmacology · doi:10.1016/s0014-2999(00)00639-7 · Cited by 213
Drosophila DJ-1 mutants show oxidative stress-sensitive locomotive dysfunction
Park, J., Kim, S. Y., Cha, G., Lee, S. B., Kim, S., & Chung, J. (2005) · Gene · doi:10.1016/j.gene.2005.06.040 · Cited by 219
Glutathione and Parkinson's disease: Is this the elephant in the room?
Zeevalk, G. D., Razmpour, R., & Bernard, L. P. (2008) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2008.01.017 · Cited by 217
Oxidative Stress and Neurodegenerative Disorders
Sun, A. Y., & Chen, Y. (1998) · Journal of Biomedical Science · doi:10.1007/bf02255928 · Cited by 214
Can the brain be protected through exercise? Lessons from an animal model of parkinsonism☆
Smith, A. D., & Zigmond, M. J. (2003) · Experimental Neurology · doi:10.1016/j.expneurol.2003.08.017 · Cited by 209

Authors: GRAHAM, D. G.
Affiliations: Duke Medical Center (US)
Corresponding author: GRAHAM, DOYLE G.
Venue: Molecular Pharmacology
Publisher: Elsevier BV
Published: 1978-07
Volume: 14
Issue: 4
Pages: 633-643
ISSN: 0026-895X (ISSN-L)
DOI: 10.1016/s0026-895x(25)13535-9
OpenAlex: W2211987820
Cited by: 1,126
References: 0
Citations by year: 2026: 11 · 2025: 12 · 2024: 6 · 2023: 11 · 2022: 13 · 2021: 20 · 2020: 23 · 2019: 26 · 2018: 29 · 2017: 30 · 2016: 26 · 2015: 29 · 2014: 26 · 2013: 26 · 2012: 49
FWCI: 1.86
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Molecular Pharmacology (publishedVersion)
PubMed (publishedVersion)
PubMed
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
Keywords: catecholamines, autoxidation, periodate oxidation, 6-hydroxydopamine, dopamine, norepinephrine, epinephrine, aminochrome, adrenochrome, o-quinones, p-quinones, cyclization, tautomerism, neuromelanin
MeSH terms: Catecholamines, Dopamine, Epinephrine, Hydroxydopamines, Melanins, Norepinephrine, Oxidation-Reduction, Quinones, Monophenol Monooxygenase

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

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