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GdCl3 Induced Hep G2 Cell Death through Mitochondrial and External Death Pathways without Significant Elevation of ROS Generation
Ye, Lihua1; Shi, Zhe2; Liu, Huixue2; Yang, Xiaoda1; Wang, Kui1
关键词Gadolinium Chloride Apoptosis Mitochondria Mapk
刊名BIOLOGICAL TRACE ELEMENT RESEARCH
2013
DOI10.1007/s12011-012-9538-y
151期:1页:148-155
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Endocrinology & Metabolism
研究领域[WOS]Biochemistry & Molecular Biology ; Endocrinology & Metabolism
关键词[WOS]OXIDATIVE STRESS ; INDUCED APOPTOSIS ; SIGNALING PATHWAYS ; HEPATOMA-CELLS ; NIH 3T3-CELLS ; CYTOCHROME-C ; ACTIVATION ; BAX ; MEMBRANE ; NANOPARTICLES
英文摘要

Gadolinium (Gd) compounds have important applications as MRI contrast and potential anticancer agents. The present study investigated the mechanisms of the proapoptotic effect of gadolinium chloride (GdCl3) on hepatoblastoma cell line (Hep G2) tumor cells. The experimental results indicated that GdCl3 induced apoptosis of Hep G2 at high concentration and with long time incubation; however, unlike the actions on normal cell lines, GdCl3 did not cause any oxidative stress on tumor cells. Cytochrome c (Cyt c) and apoptosis inducing factor release, Bax translocation, collapse of mitochondria membrane potential, caspase 3 and 8 activation, and Bid cleavage were observed along with a sustained activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2 terminal kinase (JNK). Addition of ERK and JNK inhibitor attenuated the effect of GdCl3 induced apoptosis and Cyt c release. All the results suggested a novel mechanism that GdCl3 induced Hep G2 cell death through intrinsic and external death pathways without significant elevation of reactive oxygen species generation. The present work provided new insight to understand the mechanisms of the biological effects of GdCl3 and implications for the development of anticancer Gd agents.

语种英语
WOS记录号WOS:000312880700020
项目编号20671008 ; 20971008
资助机构National Natural Science Foundation of China
引用统计
被引频次:4[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56730
专题北京大学药学院_化学生物学系
作者单位1.Peking Univ, State Key Labs Nat & Biomimet Drugs, Beijing 100083, Peoples R China
2.Peking Univ, Dept Biol Chem, Sch Pharmaceut Sci, Hlth Sci Ctr, Beijing 100083, Peoples R China
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Ye, Lihua,Shi, Zhe,Liu, Huixue,et al. GdCl3 Induced Hep G2 Cell Death through Mitochondrial and External Death Pathways without Significant Elevation of ROS Generation[J]. BIOLOGICAL TRACE ELEMENT RESEARCH,2013,151(1):148-155.
APA Ye, Lihua,Shi, Zhe,Liu, Huixue,Yang, Xiaoda,&Wang, Kui.(2013).GdCl3 Induced Hep G2 Cell Death through Mitochondrial and External Death Pathways without Significant Elevation of ROS Generation.BIOLOGICAL TRACE ELEMENT RESEARCH,151(1),148-155.
MLA Ye, Lihua,et al."GdCl3 Induced Hep G2 Cell Death through Mitochondrial and External Death Pathways without Significant Elevation of ROS Generation".BIOLOGICAL TRACE ELEMENT RESEARCH 151.1(2013):148-155.
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