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Bisphenol A inhibits proliferation and induces apoptosis in micromass cultures of rat embryonic midbrain cells through the JNK, CREB and p53 signaling pathways
Liu, Ran; Xing, Lina; Kong, Dan; Jiang, Jianjun; Shang, Lanqin; Hao, Weidong
关键词Bisphenol A Micromass culture Developmental toxicity Apoptosis Cell cycle
刊名FOOD AND CHEMICAL TOXICOLOGY
2013-02-01
DOI10.1016/j.fct.2012.10.033
52页:76-82
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Food Science & Technology ; Toxicology
研究领域[WOS]Food Science & Technology ; Toxicology
关键词[WOS]EXPOSURE ; TOXICITY ; BPA
英文摘要

Bisphenol A (BPA) has been widely used in the manufacture of polycarbonate plastic, water bottles and food containers. Previous studies have established that BPA could cause developmental toxicity by inhibiting the proliferation and differentiation of rat embryonic midbrain (MB) cells in vitro. However, the underlying mechanisms have not been well studied yet. In the current study, we examined the proliferation and differentiation of MB cells treated with 10(-12)-10(-4) M BPA and found that only 10(-4) M BPA inhibited proliferation and differentiation. Then, we investigated the cell cycle progression and apoptosis of MB cells; 10(-4) M BPA caused an explicit S phase and G2/M phase arrest in the cell cycle and increased the percentage of apoptotic cells. Moreover, the phosphorylation of mitogen-activated protein kinase (MAPK) and cyclic-AMP response binding protein (CREB) and the expression of some apoptotic regulatory genes were investigated. BPA (10(-4) M) reduced the phosphorylation of C-Jun N-terminal kinase (JNK) and CREB, and increased the mRNA expression level of Bax and p53. Our findings demonstrated that BPA could cause developmental toxicity through anti-proliferation and pro-apoptosis in MB cells. Multiple signaling pathways, such as the JNK, CREB and p53-mitochondrial apoptosis pathways, participate in these effects. (C) 2012 Elsevier Ltd. All rights reserved.

语种英语
WOS记录号WOS:000314482300010
项目编号30972501 ; 2006BKA02A02 ; 2009ZX09301-010
资助机构National Natural Sciences Foundations of the People&prime ; s Republic of China ; Key Projects in the National Science and Technology Pillar Program in the Eleventh Five-year Plan Period ; National Science and Technology Major Specific Project
引用统计
被引频次:25[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/400002259/64203
专题北京大学公共卫生学院_公共卫生学院
北京大学公共卫生学院_毒理学系
作者单位Peking Univ, Sch Publ Hlth, Dept Toxicol, Beijing Key Lab Toxicol Res & Risk Assessment Foo, Beijing 100191, Peoples R China
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Liu, Ran,Xing, Lina,Kong, Dan,et al. Bisphenol A inhibits proliferation and induces apoptosis in micromass cultures of rat embryonic midbrain cells through the JNK, CREB and p53 signaling pathways[J]. FOOD AND CHEMICAL TOXICOLOGY,2013,52:76-82.
APA Liu, Ran,Xing, Lina,Kong, Dan,Jiang, Jianjun,Shang, Lanqin,&Hao, Weidong.(2013).Bisphenol A inhibits proliferation and induces apoptosis in micromass cultures of rat embryonic midbrain cells through the JNK, CREB and p53 signaling pathways.FOOD AND CHEMICAL TOXICOLOGY,52,76-82.
MLA Liu, Ran,et al."Bisphenol A inhibits proliferation and induces apoptosis in micromass cultures of rat embryonic midbrain cells through the JNK, CREB and p53 signaling pathways".FOOD AND CHEMICAL TOXICOLOGY 52(2013):76-82.
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