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壬基酚对Sprague-Dawley大鼠支持细胞诱导变化的蛋白质组学分析。

Proteomic analysis of changes induced by nonylphenol in Sprague-Dawley rat Sertoli cells.

作者信息

Wu Jiang, Wang Fuqiang, Gong Yi, Li Dongmei, Sha Jiahao, Huang Xiaoyan, Han Xiaodong

机构信息

Immunology and Reproductive Biology Laboratory, Medical School, Nanjing University, Nanjing, 210093, PR China.

出版信息

Chem Res Toxicol. 2009 Apr;22(4):668-75. doi: 10.1021/tx800406z.

Abstract

Nonylphenol (NP) is a common environmental contaminant that is known to disrupt the reproductive system. The testicular Sertoli cells play a pivotal role in the regulation of spermatogenesis and are susceptible to NP-induced reproductive lesions. Our goal was to ascertain whether NP could induce apoptosis in Sertoli cells and to explore the preapoptotic changes in Sertoli cells at low NP concentrations, similar to environmental conditions. In order to survey events that occur at the protein level in Sertoli cells after exposure to NP, we used a proteomic approach with two-dimensional gel electrophoresis (2DE) and mass spectrometry to identify proteins with altered expression in rat Sertoli cells treated with 0.01 and 0.1 microM NP for 24 h. We separated 63 protein spots and identified 41 that were differently expressed in the NP-treated groups and the control. Of these 41 spots, we focused on Raf kinase inhibitor protein (RKIP), Annexin A7 (ANXA7), ERp57, and Peroxiredoxin 6 (PRDX6) for further analysis by Western blot. These proteins are involved in the response of Sertoli cells to programmed cell death. These data help to outline mechanisms by which NP might induce apoptotic tendencies in Sertoli cells.

摘要

壬基酚(NP)是一种常见的环境污染物,已知会扰乱生殖系统。睾丸支持细胞在精子发生的调节中起关键作用,并且易受NP诱导的生殖损伤影响。我们的目标是确定NP是否能诱导支持细胞凋亡,并探索在低NP浓度下(类似于环境条件)支持细胞的凋亡前变化。为了研究NP暴露后支持细胞中蛋白质水平发生的事件,我们采用蛋白质组学方法,通过二维凝胶电泳(2DE)和质谱来鉴定在0.01和0.1微摩尔NP处理24小时的大鼠支持细胞中表达发生改变的蛋白质。我们分离出63个蛋白质斑点,并鉴定出41个在NP处理组和对照组中差异表达的斑点。在这41个斑点中,我们重点关注Raf激酶抑制蛋白(RKIP)、膜联蛋白A7(ANXA7)、内质网蛋白57(ERp57)和过氧化物酶体增殖物激活受体6(PRDX6),通过蛋白质免疫印迹法进行进一步分析。这些蛋白质参与支持细胞对程序性细胞死亡的反应。这些数据有助于勾勒出NP可能诱导支持细胞凋亡倾向的机制。

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