Oxidative Pathways for Catecholamines in the Genesis of Neuromelanin, Cytotoxic Quinones and Superoxide (O2) and Hydroxide (Oh.) Radicals

Graham, Doyle G.

doi:10.1097/00005072-197809000-00155

Cited by 431 publications

(653 citation statements)

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“…Therefore brain is a more susceptible target of free radical damage. The recent hypothesis that free radicals may be involved in the pathogenesis of certain CNS diseases has gained increasing popularity in recent years ( 6,7,8,9).…”

Section: Introductionmentioning

confidence: 99%

Oxidative injury and antioxidant vitamins E and C in Schizophrenia

D’Souza

2003

Indian J Clin Biochem

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Susceptibility of Schizophrenic patients to lipid peroxidation relative to healthy control subjects was investigated by measuring the malondialdehyde (MDA) levels in plasma. The main finding was that Schizophrenic patients were more susceptible than control subjects to oxidative damage as evident from increased MDA levels in plasma. Antioxidant levels are also depleted in Schizophrenic patients when compared to normal subjects as evident from decreased levels of vitamins E and C in the plasma. Impaired antioxidant defense and increased lipid peroxidation suggests that treatment with antioxidants (Vitamin E, Vitamin C, beta carotene) at the initial stages of illness may prevent further oxidative injury and deterioration of associated neurological deficits in Schizophrenia.

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Section: Introductionmentioning

confidence: 99%

Oxidative injury and antioxidant vitamins E and C in Schizophrenia

D’Souza

2003

Indian J Clin Biochem

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“…The brains of PD patients also show evidence of impaired proteasomal function [6], a defect that results in increased oxidative stress and decreased elimination of oxidatively damaged polypeptides [7][8][9]. Dopaminergic neurons of the substantia nigra contain relatively high basal levels of ROS resulting from dopamine metabolism and auto-oxidation [10]. Therefore, these neurons may be selectively vulnerable to insults that increase oxidative stress in PD, including complex I inhibition and proteasome impairment.…”

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confidence: 99%

Methionine sulfoxide reductase A protects dopaminergic cells from Parkinson's disease-related insults

Liu

Hindupur

Nguyen

et al. 2008

Free Radical Biology and Medicine

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Parkinson's disease (PD) is a neurologic disorder characterized by dopaminergic cell death in the substantia nigra. PD pathogenesis involves mitochondrial dysfunction, proteasome impairment, and α-synuclein aggregation, insults that may be especially toxic to oxidatively stressed cells including dopaminergic neurons. The enzyme methionine sulfoxide reductase A (MsrA) plays a critical role in the antioxidant response by repairing methionine-oxidized proteins and by participating in cycles of methionine oxidation and reduction that have the net effect of consuming reactive oxygen species. Here, we show that MsrA suppresses dopaminergic cell death and protein aggregation induced by the complex I inhibitor rotenone or mutant α-synuclein, but not by the proteasome inhibitor MG132. By comparing the effects of MsrA and the small-molecule antioxidants N-acetyl-cysteine and vitamin E, we provide evidence that MsrA protects against PD-related stresses primarily via methionine sulfoxide repair rather than by scavenging reactive oxygen species. We also demonstrate that MsrA efficiently reduces oxidized methionine residues in recombinant α-synuclein. These findings suggest that enhancing MsrA function may be a reasonable therapeutic strategy in PD. Keywords aggresome; dopamine; glutathione; heat shock protein; methionine sulfoxide reductase; neurodegeneration; oxidative stress; Parkinson's disease; proteasome; protofibril; rotenone; synuclein Parkinson's disease (PD) is a neurologic disorder that involves a selective loss of dopaminergic neurons from the substantia nigra [1,2]. The postmortem brains of PD patients are characterized by reduced activity of mitochondrial complex I, an enzyme of the mitochondrial electron transport chain [3,4]. In turn, this defect may cause a 'leakage' of electrons from mitochondria, leading to the accumulation of reactive oxygen species (ROS) that damage *Corresponding author. Address: Jean-Christophe Rochet, Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, 575 Stadium Mall Drive, RHPH 410A, West Lafayette, Indiana, 47907-209147907- . Fax: 765-494-1414. E-mail: rochet@pharmacy.purdue.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptFree Radic Biol Med. Author manuscript; available in PMC 2009 August 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript proteins, lipids, and nucleic acids [3,5]. The brains of PD patients also show evidence of impaired proteasomal function [6], a defect that results in increased oxidative stress and decreased elimination...

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“…For example, substantial increases in dopamine levels in this brain region were reported following 10 minutes of arterial occlusion, which then returned to baseline levels after 60 minutes (40). However, other studies have reported that dopamine protects neurons against glutamate-induced excitotoxicity (37) and that dopamine levels are reduced following ischemia (38)(39)(40). In addition, it has been shown that some experimental conditions can lead to increased TH levels in the striatum (21), suggesting the existence of tissue-specific modulation.…”

Section: Discussionmentioning

confidence: 97%

“…Existing data point to increased levels of dopamine during ischemia (34,35), particularly in the neostriatum (18,(36)(37)(38)(39). For example, substantial increases in dopamine levels in this brain region were reported following 10 minutes of arterial occlusion, which then returned to baseline levels after 60 minutes (40).…”

Section: Discussionmentioning

confidence: 99%

La atorvastatina protege las neuronas GABAérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

et al. 2014

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Author contributions:Angélica María Sabogal: conducted the experiments, collected and discussed results, and prepared the manuscript. César Augusto Arango: consulted on cerebral ischemia procedures and nigrostriatal physiology; discussed results and reviewed the manuscript. Gloria Patricia Cardona: managed and supervised experiments; reviewed scientific merit; performed input protein analysis; reviewed, revised and approved the manuscript; submitted the manuscript. Ángel Enrique Céspedes: approved the project; managed and supervised the study; analyzed and interpreted the results, discussions and conclusions; reviewed and approved the manuscript. Introduction: Cerebral ischemia is the third leading cause of death and the primary cause of permanent disability worldwide. Atorvastatin is a promising drug with neuroprotective effects that may be useful for the treatment of stroke. However, the effects of atorvastatin on specific neuronal populations within the nigrostriatal system following cerebral ischemia are unknown. Objective: To evaluate the effects of atorvastatin on dopaminergic and GABAergic neuronal populations in exofocal brain regions in a model of transient occlusion of the middle cerebral artery. Materials and methods: Twenty-eight male eight-week-old Wistar rats were used in this study. Both sham and ischemic rats were treated with atorvastatin (10 mg/kg) or carboxymethylcellulose (placebo) by gavage at 6, 24, 48 and 72 hours post-reperfusion. We analyzed the immunoreactivity of glutamic acid decarboxylase and tyrosine hydroxylase in the globus pallidus, caudate putamen and substantia nigra. Results: We observed neurological damage and cell loss in the caudate putamen following ischemia. We also found an increase in tyrosine hydroxylase immunoreactivity in the medial globus pallidus and substantia nigra reticulata, as well as a decrease in glutamic acid decarboxylase immunoreactivity in the lateral globus pallidus in ischemic animals treated with a placebo. However, atorvastatin treatment was able to reverse these effects, significantly decreasing tyrosine hydroxylase levels in the medial globus pallidus and substantia nigra reticulata and significantly increasing glutamic acid decarboxylase levels in the lateral globus pallidus. Conclusion: Our data suggest that post-ischemia treatment with atorvastatin can have neuroprotective effects in exofocal regions far from the ischemic core by modulating the GABAergic and dopaminergic neuronal populations in the nigrostriatal system, which could be useful for preventing neurological disorders. Atorvastatin protectsKey words: GABAergic neurons, dopaminergic neurons, brain ischemia; models, animal; rats. doi: http://dx.doi.org/10.7705/biomedica.v34i2.1851La atorvastatina protege las neuronas gabérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas Introducción. La isquemia cerebral es la tercera causa de muerte y la primera de discapacidad permanente en el mundo. La atorvastatina es un fárm...

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Oxidative Pathways for Catecholamines in the Genesis of Neuromelanin, Cytotoxic Quinones and Superoxide (O2) and Hydroxide (Oh.) Radicals

Cited by 431 publications

References 0 publications

Oxidative injury and antioxidant vitamins E and C in Schizophrenia

Oxidative injury and antioxidant vitamins E and C in Schizophrenia

Methionine sulfoxide reductase A protects dopaminergic cells from Parkinson's disease-related insults

La atorvastatina protege las neuronas GABAérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

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