E2弱化双酚A雌激素活性机制  

Mechanisms of E2 weakening effects on BPA's estrogenicity

作　　者：张光明[1,2] 郎朗[1,3] 李钰[4] 马军[1] 

机构地区：[1]哈尔滨工业大学市政环境工程学院,哈尔滨150090 [2]中国人民大学环境学院,北京100872 [3]哈尔滨商业大学生命与环境科学研究中心,哈尔滨150028 [4]哈尔滨工业大学理学院,哈尔滨150001

出　　处：《哈尔滨工业大学学报》2012年第4期28-31,共4页Journal of Harbin Institute of Technology

基　　金：国家高技术研究发展计划项目(2007AA06Z339);水体污染控制与治理科技重大专项课题(2009ZX07424-005)

摘　　要：前期研究发现天然雌激素E2可以弱化一种常见雌激素类污染物双酚A的活性,为探讨这一现象的机制,利用人体乳腺癌细胞MCF-7,从细胞周期、雌激素受体途径、MAPKs信号途径进行实验.结果表明:E2可诱导DNA合成期细胞显著增高,抑制受体蛋白表达,提高ERK蛋白的表达,进而激活多种转录因子;双酚A显著抑制受体蛋白表达,对MAPKs信号通路基本没有影响,可同时提高DNA分裂期与间歇期细胞比例;两者联合后活化了受体途径和ERK途径,促进C-fos的转录表达,激活cyclin D1蛋白,增加S期及G2期细胞比例.E2弱化双酚A的可能机制为C-myc蛋白表达下降.Previous study showed that natural estrin, 17-Estradiol （E2）, could weaken the estrogenicity of Bi- sphenol A （BPA）, a common estrin in water resources. In order to learn the potential mechanisms, experi- ments were performed with human breast cancer cell MCF-7 on the cell cycle, estrogen receptor pathway and MAPKs pathway. Results showed that E2 worked through estrogen receptors and ERK pathway, and activated C-myc gene, C-fos gene, and cyclin D1 protein, and thus increased the S section of the cell cycle. BPA worked mainly through estrogen receptors by activating cyclin D1 protein, and increased the S and G2 sections of the cell cycle. The mixture of BPA and E2 worked through both pathways, activated both C-fos and cyclin D1, and increased both S and G2 sections of the cell cycle. The main mechanism of E2＇ s weakening on BPA＇ s estrogenicity might be the decreased expression of C-myc protein.

关 键 词：雌二醇 双酚A 雌激素活性 C-MYC蛋白表达 细胞周期 

分 类 号：X703.1[环境科学与工程—环境工程]