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Inhibition of hydrogen sulfide generation contributes to 1-methy-4-phenylpyridinium ion-induced neurotoxicity

txq01001 添加于 2011-2-15 07:07 | 1719 次阅读 | 0 个评论

作者
Tang X-Q, Fan L-L, Li Y-J, Shen X-T, Zhuan Y-Y, He J-Q, Xu J-H, Hu B, Li Y-J
摘要
Reactive oxygen species (ROS) overproduction contributes to the neurotoxicity of 1-methy-4-phenylpyridinium ion (MPP(+)). Increasing studies have shown that hydrogen sulfide (H(2)S) is an endogenous antioxidant gas. We have hypothesized that MPP(+)-caused neurotoxicity may involve the imbalance of proportion to this endogenous protective antioxidant gas. The aim of this study is to evaluate whether MPP(+) disturbs H(2)S synthesis in PC12 cells, a clonal rat pheochromocytoma cell line, and whether disturbance of H(2)S generation induced by MPP(+) is an underlying mechanism of MPP(+)-induced neurotoxicity. We show that exposure of PC12 cells to MPP(+) causes a significant decrease in H(2)S generation and results in remarkable cell damage. We find that cystathionine-beta-synthetase (CBS) is catalyzed in PC12 cells to generate H(2)S, and that both expression and activity of CBS are inhibited by MPP(+) treatment. Exposure of sodium hydrosulfide (NaHS), a donor of H(2)S, extenuates MPP(+)-induced cytotoxicity and ROS accumulation in PC12 cells, while inhibition of CBS by amino-oxyacetate (AOAA) exacerbates the effects of MPP(+). These results indicate that MPP(+) neurotoxicity involves reduction of H(2)S production, which is caused by inhibition of CBS. This study provides novel insights into cell death observed in neurodegenerative disease such as Parkinson's disease.
详细资料
- 文献种类:期刊
- 期刊名称: Neurotoxicity Research
- 期刊缩写: Neurotox Res
- 期卷页: 2011年第19卷第3期 403-411页
- 地址: Department of Physiology, Medical College, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, People's Republic of China, txq01001@gmail.com
- ISBN: 1029-8428
- 备注:PMID:20361290
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附件
Inhibition of hydrogen sulfide generation contributes to 1-methy-4-phenylpyridin