Volume 24, Issue. 2, April, 2008


Mitochondria dysfunction was involved in copper-induced toxicity in MES23.5 cells

 Li-Min SHI, Hong JIANG, Jun WANG, Ze-Gang MA, Jun-Xia XIE  


State Key Disciplines: Physiology (in incubation), Department of Physiology, Qingdao University, Qingdao 266071,China

Abstract 

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 μmol/L copper had no effect on the MES23.5 cell viability, whereas 400 and 800 μmol/L of copper could decrease the cell viability (P < 0.01). Treating cells with 200 μmol/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 μmol/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.

Keywords

copper; dopamine; mitochondria

[SpringerLink]