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Apoptosis induced by cadmium in human lymphoma U937 cells through Ca2+-calpain and caspase-mitochondria dependent pathways
Li, M; Kondo, T; Zhao, QL; Li, FJ; Tanabe, K; Arai, Y; Zhou, ZC; Kasuya, M
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2000-12-15
275期:50页:39702-39709
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR ; CYTOCHROME-C RELEASE ; DNA FRAGMENTATION ; T-CELLS ; BCL-X ; CALCIUM ; DEATH ; ACTIVATION ; INDUCTION ; PROTEIN
英文摘要

Apoptosis induced by cadmium has been shown in many tissues in vivo and in cultured cells in vitro. However, its molecular mechanism is not fully understood. When the human histiocytic lymphoma cell line U937 was treated with cadmium for 12 h, evidence of apoptotic features, including change in nuclear morphology, DNA fragmentation, formation of DNA ladder in agarose gel electrophoresis, and phosphatidylserine externalization, were obtained. Moreover, loss of the mitochondrial membrane potential (Delta psi (m)) was observed in the cadmium-treated cells and was inhibited by a broad caspase inhibitor (Z-VAD-FMK). Caspase inhibitors suppressed the DNA fragmentation in the order of Z-VAD-FMK > caspase-8 inhibitor > caspase-3 inhibitor. Expression of Bcl-x(L) and Bid decreased significantly in the cadmium-treated cells, although no apparent change in Bcl-2 and Bax expression was found. Tetrakis-(2-pyridylmethyl) ethylendiamine, a cell-permeable heavy metal chelator, partially reversed the increase of fluorescence of Fura-a in the cadmium-treated cells. In addition, verapamil (70 muM), a voltage-dependent Ca2+ channel blocker, inhibited the DNA fragmentation induced by cadmium less than 100 muM and decreased the fluorescence of Fura-8. Cadmium up-regulated the expression of type 1 inositol 1,4,5-trisphosphate receptor (IP3R) but not type 2 or type 3 IP3R Calpain inhibitors I and II partially prevented DNA fragmentation. No effects of Z-VAD-FMK on the expression of type 1 IP3R or of calpain inhibitors on the loss of Delta psi (m) were observed. These results suggest that cadmium possibly induced apoptosis in U937 cells through two independent pathways, the Ca2+-calpain-dependent pathway and the caspase-mitochondria-dependent pathway.

语种英语
WOS记录号WOS:000165953100099
引用统计
被引频次:185[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/400002259/54059
专题北京大学公共卫生学院_毒理学系
作者单位1.Toyama Med & Pharmaceut Univ, Fac Med, Dept Radiol Sci, Sugitani, Toyama 9300197, Japan
2.Toyama Med & Pharmaceut Univ, Fac Med, Dept Publ Hlth, Sugitani, Toyama 9300197, Japan
3.Beijing Med Univ, Sch Publ Hlth, Dept Toxicol, Beijing 100083, Peoples R China
4.China Med Univ, Sch Publ Hlth, Dept Ind Hyg & Occupat Dis, Shenyang 110001, Peoples R China
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GB/T 7714
Li, M,Kondo, T,Zhao, QL,et al. Apoptosis induced by cadmium in human lymphoma U937 cells through Ca2+-calpain and caspase-mitochondria dependent pathways[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2000,275(50):39702-39709.
APA Li, M.,Kondo, T.,Zhao, QL.,Li, FJ.,Tanabe, K.,...&Kasuya, M.(2000).Apoptosis induced by cadmium in human lymphoma U937 cells through Ca2+-calpain and caspase-mitochondria dependent pathways.JOURNAL OF BIOLOGICAL CHEMISTRY,275(50),39702-39709.
MLA Li, M,et al."Apoptosis induced by cadmium in human lymphoma U937 cells through Ca2+-calpain and caspase-mitochondria dependent pathways".JOURNAL OF BIOLOGICAL CHEMISTRY 275.50(2000):39702-39709.
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