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dc.contributor.authorCai, Jiali
dc.contributor.authorWang, Mengmeng
dc.contributor.authorLi, Bowen
dc.contributor.authorWang, Chonggang
dc.contributor.author王重刚
dc.contributor.authorChen, Yixin
dc.contributor.authorZuo, Zhenghong
dc.contributor.author左正宏
dc.date.accessioned2011-08-15T13:30:42Z
dc.date.available2011-08-15T13:30:42Z
dc.date.issued2009
dc.identifier.citationCHEMICAL RESEARCH IN TOXICOLOGY,2009, 22 (9), pp 1582–1587zh_CN
dc.identifier.issn0893-228X
dc.identifier.urihttp://dx.doi.10.1021/tx900120z
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/10424
dc.description.abstractIn evaluating the cytotoxic effects and the mechanisms of the apoptotic and necrotic actions of trimethyltin chloride (TMT) on human hepatoma G2 (HepG2) cells, the present Study focused on the involvement of antiproliferation, DNA damage, cell death, apoptosis-related proteins, and p53-dependent transcriptional activity. Twenty-four hour TMT treatments (4-64, mu M) induced apoptosis and necrosis in HepG2 cells. Thirty-two micromolar and higher concentration significantly increases cell death. DNA damage was observed at 8 mu M. Additionally, TMT increased the activity Of cellular caspase-3 and the release of mitochondrial cytochrome c in a concentration-dependent manner. Our data demonstrated that the Bcl-2 family of proteins was involved in the apoptotic process but that p53 expression level was not affected. the results Of luciferase reporter assay indicated that TMT-induced apoptosis seemed to adopt a transcription-dependent route, by activating p53 target genes such as PUMA and p21.zh_CN
dc.language.isoenzh_CN
dc.publisherAMER CHEMICAL SOCzh_CN
dc.titleApoptotic and Necrotic Action Mechanisms of Trimethyltin in Human Hepatoma G2 (HepG2) Cellszh_CN
dc.typeArticlezh_CN


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