| Iron contributes to the formation of catechol isoquinolines and oxidative toxicity induced by overdose dopamine in dopaminergic SH-SY5Y cells. | |
| | |
MedLine Citation:
|
PMID: 18500384 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
OBJECTIVE: The selective loss of dopaminergic neurons in Parkinson's disease is suspected to correlate with the increase of cellular iron, which may be involved in the pathogenesis of PD by promotion of oxidative stress. This research investigated dopamine-induced oxidative stress toxicity contributed by iron and the production of dopamine-derived neurotoxins in dopaminergic SH-SY5Y cells. METHODS: After the SH-SY5Y cells were pre-incubated with dopamine and Fe2+ for 24 h, the cell viability, hydroxyl radical, melondialdehyde, cell apoptosis, and catechol isoquinolines were measured by lactate dehydrogenase assay, salicylic acid trapping method, thiobarbuteric acid assay, Hoechst 33258 staining and HPLC-electrochemical detection (HPLC-ECD), respectively. RESULTS: (1) Optimal dopamine (150 micromol/L) and Fe2+ (40 or 80 micromol/L) significantly increased the concentrations of hydroxy radicals and melondialdehyde in SH-SY5Y cells. (2) Induction with dopamine alone or dopamine and Fe2+ (dopamine/Fe2+) caused cell apoptosis. (3) Compared with untreated cells, the catechol isoquinolines, salsolinol and N-methyl-salsolinol in dopamine/Fe2+-induced cells were detected in increasing amounts. CONCLUSION: Due to dopamine/Fe2+-induced oxidative stress similar to the state in the parkinsonian substantia nigra neurons, dopamine and Fe2+ impaired SH-SY5Y cells could be used as the cell oxidative stress model of Parkinson's disease. The catechol isoquinolines detected in cells may be involved in the pathogenesis of Parkinson's disease as potential neurotoxins. |
| | |
Authors:
|
Ran Wang; Hong Qing; Xiao-Qian Liu; Xiao-Lin Zheng; Yu-Lin Deng |
Related Documents
:
|
239654 - Study of the regulation of oxidation and co2 assimilation in intact nitrobacter winogra... 17882254 - Nitric oxide in the central nervous system: neuroprotection versus neurotoxicity. 7928464 - Role of gamma-glutamyltranspeptidase-mediated glutathione transport on the radiosensiti... 36614 - Translocation of glutathione from lymphoid cells that have markedly different gamma-glu... 6195164 - Phosphorylation of keratin and vimentin polypeptides in normal and transformed mitotic ... 21631944 - Mhc class i-related chain a and b ligands are differentially expressed in human cervica... |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Neuroscience bulletin Volume: 24 ISSN: 1673-7067 ISO Abbreviation: - Publication Date: 2008 Jun |
Date Detail:
|
Created Date: 2008-05-26 Completed Date: 2008-08-21 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101256850 Medline TA: Neurosci Bull Country: China |
Other Details:
|
Languages: eng Pagination: 125-32 Citation Subset: IM |
Affiliation:
|
School of Life Science and Technology, Beijing Institute of Technology, Beijing, China. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Apoptosis
/
drug effects,
physiology Catechols / metabolism Cell Line, Tumor Cell Survival / drug effects, physiology Dopamine / toxicity* Dose-Response Relationship, Drug Humans Hydroxyl Radical / metabolism Iron / metabolism* Iron Metabolism Disorders / complications, metabolism, physiopathology Isoquinolines / metabolism* Malondialdehyde / metabolism Models, Biological Nerve Degeneration / chemically induced, metabolism*, physiopathology Neurons / drug effects, metabolism* Neurotoxins / toxicity Oxidative Stress* / drug effects Parkinson Disease / etiology, metabolism, physiopathology Salsoline Alkaloids / metabolism Up-Regulation / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
|
0/Catechols; 0/Isoquinolines; 0/Neurotoxins; 0/Salsoline Alkaloids; 3352-57-6/Hydroxyl Radical; 525-72-4/salsolinol; 542-78-9/Malondialdehyde; 7439-89-6/Iron; 89-31-6/salsoline |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Gene doping: the hype and the reality.
Next Document: Triptolide protects against 1-methyl-4-phenyl pyridinium-induced dopaminergic neurotoxicity in rats:...