BACKGROUND: Aggregation of α-synuclein is the major component of Lewy bodies, which are the pathological hallmarks of Parkinson disease (PD). Although the mechanism of this protein aggregates is unclear, previous study showed that environmental toxins such as rotenone could induce the expression and aggregation of α-synuclein. OBJECTIVE: To observe the role of α-synuclein in PD. DESIGN: A randomized controlled trial. SETTING: Beijing Institute for Neuroscience, Capital University of Medical Sciences. MATERIALS: This study was performed from July 2005 to January 2006 at the Beijing Institute for Neuroscience, Capital University of Medical Sciences. Human dopaminergic neuroblastoma SH-SY5Y cells were provided by Beijing Institute for Neuroscience, Capital University of Medical Sciences. METHODS: Human dopaminergic neuroblastoma SH-SY5Y cells were treated to make α-synuclein over express. Rotenone was added into the medium of cultured both native SH-SY5Y cells and α-synuclein-overexpression SH-SY5Y cells. Lactate dehydrogenase (LDH) assay was used to detect with the cell viability. Flow cytometry and electrophoresis were adopted to measure the cell apoptosis. MAIN OUTCOME MEASURES: Cell viability, DNA fragmentation, and the number of cell apoptosis. RESULTS: After being treated with rotenone, LDH activity of α-synuclein overexpressed SH-SY5Y cells was (76.625±6.34) μkat/L, which was significantly lower than that of control group (P < 0.05). As compared with normal SH-SY5Y cell, α-synuclein over-expressed SH-SY5Y cells had less DNA fragments and apoptotic cells. α-synuclein might play a role in cell apoptosis induced by rotenone, which was also confirmed by using of antioxidant reagent. CONCLUSION: α-synuclein may partially protect against cell apoptosis induced by rotenone in SH-SY5Y cells. BACKGROUND: Aggregation of α-synuclein is the major component of Lewy bodies, which are the pathological hallmarks of Parkinson disease (PD). Although the mechanism of this protein aggregates is unclear, previous study showed that environmental toxins such as rotenone could induce the expression SETJ: Beijing Institute for Neuroscience, Capital University of Medical Sciences. MATERIALS: This study was performed from July 2005 to January 2006 at the Beijing Institute for Neuroscience, Capital University of Medical Sciences. Human dopaminergic neuroblastoma SH-SY5Y cells were provided by Beijing Institute for Neuroscience, Capital University of Medical Sciences. METHODS: Human dopaminergic neuroblastoma SH-SY5Y cells were treated to make α -synuclein over express. Rotenone was added into the medium of cultured both native SH-SY5Y cells and α-synuclein-overexp Flow cytometry and electrophoresis were taken to measure the cell apoptosis. MAIN OUTCOME MEASURES: Cell viability, DNA fragmentation, and the number of cell apoptosis. ression SH-SY5Y cells. Lactate dehydrogenase (LDH) assay was used to detect with the cell viability. RESULTS: After being treated with rotenone, LDH activity of a-synuclein overexpressed SH-SY5Y cells was (76.625 ± 6.34) μkat / L, which was significantly lower than that of control group (P <0.05). As compared with normal SH- SY5Y cell, α-synuclein over-expressed SH-SY5Y cells had less DNA fragments and apoptotic cells. Α-synuclein might play a role in cell apoptosis induced by rotenone, which was also confirmed by using an antioxidant reagent. may partially protect against cell apoptosis induced by rotenone in SH-SY5Y cells.