Document Detail

Mitochondria dysfunction was involved in copper-induced toxicity in MES23.5 cells.
MedLine Citation:
PMID:  18369386     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To investigate the toxicity of copper on MES23.5 dopaminergic cells and the probable mechanisms involved in this process. METHODS: MES23.5 dopaminergic cells were selected as our experimental model. [3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide] (MTT) assay was used to detect the influence of copper on the cell viability. The semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), Western blotting and the high performance liquid chromatography-electrochemical detection (HPLC-ECD) have been used to detect the tyrosine hydroxlase (TH) mRNA and protein expression and the dopamine content in MES23.5 cells. The flow cytometry have been used to detect the changes of mitochondrial transmembrane potential. RESULTS: 100 and 200 mumol/L copper had no effect on the MES23.5 cell viability, whereas 400 and 800 mumol/L of copper could decrease the cell viability (P < 0.01). Treating cells with 200 mumol/L copper for 24 h decreased the TH mRNA expression, the TH expression and the dopamine content compared with the control (P < 0.01, P < 0.01, P < 0.05, respectively). Besides, the mitochondrial transmembrane potential also decreased with the treatment of 200 mumol/L copper for 24 h (P < 0.01). CONCLUSION: Copper could exert the toxic effects on MES23.5 dopaminergic cells and decrease the cell function. The dysfunction of mitochondria may be the mechanism of this toxicity effect.
Li-Min Shi; Hong Jiang; Jun Wang; Ze-Gang Ma; Jun-Xia Xie
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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 Apr 
Date Detail:
Created Date:  2008-03-28     Completed Date:  2008-08-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101256850     Medline TA:  Neurosci Bull     Country:  China    
Other Details:
Languages:  eng     Pagination:  79-83     Citation Subset:  IM    
State Key Disciplines: Physiology (in incubation), Department of Physiology, Qingdao University, Qingdao 266071 China.
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MeSH Terms
Cell Survival / drug effects,  genetics
Cells, Cultured
Copper / metabolism,  toxicity*
Dopamine / biosynthesis
Dose-Response Relationship, Drug
Membrane Potential, Mitochondrial / drug effects,  genetics
Mitochondria / drug effects*,  metabolism,  pathology
Nerve Degeneration / chemically induced*,  metabolism,  physiopathology
Neurons / drug effects*,  metabolism,  pathology
Neurotoxins / toxicity
Oxidative Stress / drug effects*,  physiology
Parkinson Disease / etiology*,  metabolism,  physiopathology
RNA, Messenger / drug effects,  metabolism
Tyrosine 3-Monooxygenase / drug effects,  genetics,  metabolism
Reg. No./Substance:
0/Neurotoxins; 0/RNA, Messenger; 7440-50-8/Copper; EC 3-Monooxygenase

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