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Both genetic and environmental factors are involved in the pathogenesis of Parkinson’s disease (PD). Epidemiological studiesshowed that environmental factors shared with the common mechanisms of resulting in α-synuclein aggregation by inhibiting complexI of mitochondria and leading to oxidative stress. To investigate the relationship between α-synuclein and oxidative stress, we used humandopaminergic SH-SY5Y cells transfected with α-synuclein-enhanced green fluorescent protein (EGFP). α-synuclein gene expression wasdetermined by immunocytochemistry and real-time quantitative PCR. Both SH-SY5Y and α-synuclein overexpressed SH-SY5Y (SHSY5Y/Syn) cells were treated with various concentrations of rotenone for different time. Cell viability and oxidative stress were detectedby MTT assay and DCF assay. Superoxide dismutase (SOD) activity was assessed with xanthine peroxidase method. Cell apoptosiswas detected with flow cytometry. Results showed that α-synuclein gene was constantly overexpressed in SH-SY5Y/Syn cells. Aftertreatment with rotenone, both cell viability and complex I activity in these cells were reduced in a concentration-dependent manner.Oxidative stress was also found in these cells. Compared with SH-SY5Y cells, SOD activity in SH-SY5Y/Syn cells was increased distinctly (P<0.05) and α-synuclein significantly attenuated rotenone-induced cell apoptosis. These results suggest that the α-synucleinoverexpression in SH-SY5Y cells has a tendency to partially resist oxidative stress induced by rotenone and this response may assistcell survival.