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Diethyl sulfate-induced cell cycle arrest and apoptosis in human bronchial epithelial 16HBE cells
Zhao, Peng1,2; Fu, Juanling1; Yao, Biyun1,2; Hu, Entan1; Song, Yanchao1,2; Mi, Lan1,2; Li, Zhenning1,2; Zhang, Hongtao1,2; Jia, Yongrui3; Ma, Shiliang3; Chen, Wen4; Zhou, Zongcan1
关键词Diethyl sulfate Apoptosis S arrest G2/M arrest 16HBE cells p53
刊名CHEMICO-BIOLOGICAL INTERACTIONS
2013-09-25
DOI10.1016/j.cbi.2013.06.014
205期:2页:81-89
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]Biochemistry & Molecular Biology ; Pharmacology & Pharmacy ; Toxicology
关键词[WOS]MECHANISMS ; INDUCTION ; G0/G1
英文摘要

In this study, we investigated the effects of diethyl sulfate (DES) on cell proliferation, cell cycle progression and apoptosis in human bronchial epithelial 16HBE cells. Cells were treated with various doses of DES (0, 0.5, 1.0, 2.0, 4.0 or 8.0 mM) for 12, 24 or 36 h. Cell proliferation and apoptosis were determined by MTT assay and flow cytometer, respectively. The results showed that DES inhibited cell proliferation in a dose- and time-dependent manner, and induced significant apoptosis in 16HBE cells. Apoptosis related proteins measurement results revealed that DES-induced apoptosis was concurrent with the increasing of Bax and cleavage fragment caspase-3 and the decreasing of Bcl-2 and full length procaspase-3. When cells were incubated with 2.0 mM of DES for several time intervals, S and G2/M phase accumulation was observed. Further analysis indicated that both DES-induced G1/S transition acceleration and S arrest resulted in S phase accumulation, and that DES-induced G2/M arrest resulted in G2/M phase accumulation. Western blotting results demonstrated that after DES treatment p-chk1 (Ser345) and p-chk2 (Thr68) levels decreased in G1 cells, and increased in S and G2/M cells. In addition, the increasing of chk1 and chk2 were also induced by DES treatment. With the increase in the dose of DES, p53 levels first increased (0.5-4.0 mM) and then decreased (8.0 mM). Down-regulation of p53 by RNA interference increased 4.0 mM of DES-induced apoptosis but did not affect 2.0 mM DES-induced cell cycle arrest. In conclusion, DES inhibits 16HBE cells proliferation in a dose- and time-dependent behavior. Within the sublethal dose, DES induces S and G2/M arrest through activating DNA damage checkpoints. Within the lethal dose, DES induces apoptosis through evoking apoptosis programs. p53 might play an important role in the transition between evoking cell cycle arrest/pro-survival and apoptosis programs upon DES exposure. (c) 2013 Elsevier Ireland Ltd. All rights reserved.

语种英语
WOS记录号WOS:000323993800001
项目编号81001253 ; 30972502 ; 81172693 ; 7132122 ; BMU20090460
资助机构National Nature Science Foundation of China ; Beijing Natural Science Foundation ; Fundamental Research Funds for the Central Universities
引用统计
被引频次:7[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/400002259/58527
专题北京大学公共卫生学院_毒理学系
北京大学公共卫生学院_公共卫生学院
北京大学中国卫生发展研究中心
作者单位1.Peking Univ, Dept Toxicol, Hlth Sci Ctr, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Beijing Key Lab Toxicol Res & Risk Assessment Foo, Beijing 100191, Peoples R China
3.Peking Univ, Med & Hlth Analyt Ctr, Beijing 100191, Peoples R China
4.Sun Yat Sen Univ, Sch Publ Hlth, Fac Prevent Med, Dept Toxicol, Guangzhou 510080, Guangdong, Peoples R China
推荐引用方式
GB/T 7714
Zhao, Peng,Fu, Juanling,Yao, Biyun,et al. Diethyl sulfate-induced cell cycle arrest and apoptosis in human bronchial epithelial 16HBE cells[J]. CHEMICO-BIOLOGICAL INTERACTIONS,2013,205(2):81-89.
APA Zhao, Peng.,Fu, Juanling.,Yao, Biyun.,Hu, Entan.,Song, Yanchao.,...&Zhou, Zongcan.(2013).Diethyl sulfate-induced cell cycle arrest and apoptosis in human bronchial epithelial 16HBE cells.CHEMICO-BIOLOGICAL INTERACTIONS,205(2),81-89.
MLA Zhao, Peng,et al."Diethyl sulfate-induced cell cycle arrest and apoptosis in human bronchial epithelial 16HBE cells".CHEMICO-BIOLOGICAL INTERACTIONS 205.2(2013):81-89.
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