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Alpha-Synuclein Overexpression Induced Mitochondrial Damage by the Generation of Endogenous Neurotoxins in PC12 Cells.
MedLine Citation:
PMID:  23680459     Owner:  NLM     Status:  Publisher    
Alpha-synuclein is one of the important components of Lewy body which involved in neuropathology of Parkinson's disease (PD). The relationship between α-synuclein and cell death is still unclear. In the study, PC12 cell, stably over expressing α-synuclein model was used, and we investigated the level of intracellular oxidative stress, dopamine and endogenous neurotoxin. The results showed that the level of oxidative stress and intracytoplasmic dopamine (DA) were increased in cells over expressing α-synuclein compared with normal PC12 cells. Simultaneously, additional generation of endogenous neurotoxins 1-methyl-4-phenyl-1,2,3,4-tetrahydroisoquinoline (salsolinol) and 1(R),2(N)- dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinolin (NM-salsolinol) was detected and this phenomenon was exacerbated after exposed to H2O2 for 24h, but mitigated when treated with dopamine synthesis inhibitors. The presence of endogenous neurotoxins exacerbated α-synuclein induced mitochondrial damage. These results suggest that the endogenous neurotoxins may become a bridge between α-synuclein and cell death.
Yanyan Zhang; Hong Ma; Bingjie Xie; Chao Han; Chen Wang; Hong Qing; Yulin Deng
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-5-13
Journal Detail:
Title:  Neuroscience letters     Volume:  -     ISSN:  1872-7972     ISO Abbreviation:  Neurosci. Lett.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-5-17     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7600130     Medline TA:  Neurosci Lett     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2013. Published by Elsevier Ireland Ltd.
School of Life Science, Beijing Institute of Technology, 5 South Zhongguancun Street, Haidian District, Beijing 100081, P.R. China.
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