Dual effects of α-synuclein on neurotoxicity induced by low dosage of rotenone are dependent on exposure time in dopaminergic neuroblastoma cells  

作　　者：LU LingLing,GU Li,LIANG Yuan,SUN XiaoHong,DUAN ChunLi & YANG Hui Beijing Institute for Neuroscience,Capital Medical University,The Beijing Center of Neural Regeneration and Repairingr,Key Laboratory for Neurodegenerative Disease of the Ministry of Education,Beijing 100069,China 

出　　处：《Science China(Life Sciences)》2010年第5期590-597,共8页中国科学（生命科学英文版）

基　　金：supported by the National Basic Research and Development Program of China (Grant No. 2006CB500706);the National High Technology Research and Development Program of China (Grant No. 2006AA02A408);the National Natural Science Foundation of China (Grant Nos. 30670655,30950003,30970940 and 30700199);the National Ministry of Education (Grant No. 20060025004);the Beijing Natural Science Foundation (Grant No. 5102007,5102012,7082011);the Municipal Education Commission of Beijing (Grant No. KZ201010025022);the Funding Project for Academic Human Resources Development in Institutions of Higher Learning under Jurisdiction of Beijing Municipality (Grant No. PHR200907113);the Specialized Research Fund of Excellent Talents Training of Beijing (Grant No. 20081d0501800210)

摘　　要：This study was designed to investigate the effects of α-synuclein on toxicity induced by long-term exposure to relatively low concentrations of rotenone.Compared with the control groups,the inhibition of cell viability which overexpressed α-synuclein(SH-SY5Y-Syn) improved after 1 and 2 weeks of rotenone treatment.The complex I activity was greater and the mitochondrial membrane swelling intensity was reduced after 1 and 2 weeks of treatment,which indicated that α-synuclein,at least in part,resists the rotenone-induced oxidative stress.The results indicate that α-synuclein has a dual effect on toxicity of rotenone according to exposure time in human SH-SY5Y cells.This study was designed to investigate the effects of α-synuclein on toxicity induced by long-term exposure to relatively low concentrations of rotenone.Compared with the control groups,the inhibition of cell viability which overexpressed α-synuclein(SH-SY5Y-Syn) improved after 1 and 2 weeks of rotenone treatment.The complex I activity was greater and the mitochondrial membrane swelling intensity was reduced after 1 and 2 weeks of treatment,which indicated that α-synuclein,at least in part,resists the rotenone-induced oxidative stress.The results indicate that α-synuclein has a dual effect on toxicity of rotenone according to exposure time in human SH-SY5Y cells.

关 键 词：Α-SYNUCLEIN mitochondrial DEFICIT Parkinson’s disease oxidative stress 

分 类 号：R96[医药卫生—药理学]