Differential proteomic expression of human placenta and fetal development following e-waste lead and cadmium exposure in utero
Differential proteomic expression of human placenta and fetal development following e-waste lead and cadmium exposure in utero
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子宫内电子废物铅和镉暴露后人胎盘和胎儿发育的差异蛋白质组表达
DOI：
10.1016/j.scitotenv.2015.11.084
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发表时间：
2016
影响因子：
9.8
通讯作者：
Xu Xijin
中科院分区：
文献类型：
--
作者：
Xu Long;Ge Jingjing;Huo Xia;Zhang Yuling;Lau Andy T. Y.;Xu Xijin
胎儿期铅（Pb）和镉（Cd）暴露与导致胎儿生长受限的一系列生理问题有关。本研究旨在探讨铅、镉暴露对胎盘功能的影响及其与胎儿发育的关系。胎盘标本和问卷调查收集自中国的电子废物区和参考区。采用双向电泳结合MALDI-TOF-MS/MS和分子网络关系技术对差异表达蛋白进行分析。与对照组相比，接触组胎盘铅、镉含量显著升高（p < 0.01），体长显著缩短（p < 0.01），胎龄显著增加（p < 0.01）。在线性回归模型中进行双变量调整后，体重下降205.05 g，体长下降0.44 cm，胎盘镉含量增加10 ng/g（重量）。铅呈负趋势，但缺乏统计学意义。蛋白质组学分析显示32个差异表达蛋白，主要涉及蛋白质易位、细胞骨架结构和能量代谢。富马酸水合酶在暴露的胎盘组织中下调，并通过ELISA验证。胎盘蛋白质组的改变表明，胎盘线粒体呼吸的不平衡可能是一个重要的途径，针对胎儿生长限制暴露于镉。
Prenatal exposure to lead (Pb) and cadmium (Cd) has been associated with a series of physiological problems resulting in fetal growth restriction. We aimed to investigate the effects of Pb and Cd exposure on placental function and the potential mechanisms involved in fetal development. Placental specimens and questionnaires were collected from an e-waste area and a reference area in China. Two-dimensional electrophoresis combined with MALDI-TOF-MS/MS and molecular network relationship were performed to analyze differentially expressed proteins using a compositing sample pool. Compared with the reference group, the exposed group exhibited significantly higher levels of placental Pb and Cd (p < 0.01), shorter body length and higher gestational age (p < 0.01). After bivariate adjustment in a linear regression model, decreases of 205.05 g in weight and 0.44 cm in body length were associated with a 10 ng/g wt increase in placental Cd. Pb showed a negative trend but lacked statistical significance. Proteomic analysis showed 32 differentially-expressed proteins and were predominantly involved in protein translocation, cytoskeletal structure, and energy metabolism. Fumarate hydratase was down-regulated in the exposed placenta tissues and validated by ELISA. Alterations in placental proteome suggest that imbalances in placental mitochondria respiration might be a vital pathway targeting fetal growth restriction induced by exposure to Cd.