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学科主题: 公共卫生
题名:
Diethyl sulfate-induced cell cycle arrest and apoptosis in human bronchial epithelial 16HBE cells
作者: 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
发表日期: 2013-09-25
DOI: 10.1016/j.cbi.2013.06.014
卷: 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
所属项目编号: 81001253 ; 30972502 ; 81172693 ; 7132122 ; BMU20090460
项目资助者: National Nature Science Foundation of China ; Beijing Natural Science Foundation ; Fundamental Research Funds for the Central Universities
WOS记录号: WOS:000323993800001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/58527
Appears in Collections:北京大学公共卫生学院_毒理学系_期刊论文

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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

Recommended Citation:
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.
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