Abstract：
: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-β-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.
journal_name
Neurotox Resjournal_title
Neurotoxicity researchauthors
Tang XQ,Fan LL,Li YJ,Shen XT,Zhuan YY,He JQ,Xu JH,Hu B,Li YJdoi
10.1007/s12640-010-9180-4subject
Has Abstractpub_date
2011-04-01 00:00:00pages
403-11issue
3eissn
1029-8428issn
1476-3524journal_volume
19pub_type
杂志文章abstract：:The original version of this article contained mistakes, and the authors would like to correct them. Some parts of the image in Figure 5 were missing. The correct Figure 5 is shown at the next page. ...
journal_title：Neurotoxicity research
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