Prenatal exposure to perfluorooctanesulfonate in rat resulted in long‐lasting changes of expression of synapsins and synaptophysin
Prenatal exposure to perfluorooctanesulfonate in rat resulted in long‐lasting changes of expression of synapsins and synaptophysin
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DOI：
10.1002/syn.20840
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发表时间：
2011-03
期刊：
影响因子：
2.3
通讯作者：
Huai-Cai Zeng;Yuan-yuan Li;Yuan-yuan Li;Ling Zhang;Yan-jian Wang;Jun Chen;W. Xia;Yi Lin;Jie Wei;Ziquan Lv;Miao Li;Shun‐qing Xu
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文献类型：
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作者：
Huai-Cai Zeng;Yuan-yuan Li;Yuan-yuan Li;Ling Zhang;Yan-jian Wang;Jun Chen;W. Xia;Yi Lin;Jie Wei;Ziquan Lv;Miao Li;Shun‐qing Xu
动物和人类研究都表明，在关键发育期接触化学污染物会对以后的生活产生不利影响。在子宫内，全氟辛烷磺酸（PFOS）暴露已知会导致发育神经毒性，如运动活动增加、栖息减少和认知功能受损。本研究探讨了产前全氟辛烷磺酸暴露导致认知功能受损的可能机制。妊娠Sprague道利（SD）大鼠从妊娠第0天（GD）至GD 20天通过灌胃给予0.1、0.6和2.0 mg kg−1出生体重（bw）d−1。对照组接受0.5%吐温-20溶剂（4 ml kg-1 bw d-1）。在出生后0天和21天，观察子代海马中全氟辛烷磺酸浓度。观察海马超微结构及与神经递质释放有关的突触囊泡相关蛋白的基因表达。经全氟辛烷磺酸处理的母体组的后代海马体的透射电子显微照片显示，突触的超微结构受到了负面影响。全氟辛烷磺酸处理母体组的后代在突触囊泡相关蛋白的表达方面也与对照组存在显著差异。在PND 0或PND 21，处理组中突触蛋白1（Syn 1）、突触蛋白2（Syn 2）和突触素（Syp）的mRNA水平降低。然而，PND 0时，0.6和2.0 mg kg−1组突触蛋白3（Syn 3）的mRNA水平降低，PND 21时，对照组和所有给药组之间无显著差异。这些结果提示PFOS对大鼠认知功能的损害可能与海马突触囊泡相关蛋白mRNA水平降低和突触超微结构改变有关。Synapse，2010年。© 2010 Wiley利斯公司
Both animal and human studies have demonstrated that exposure to chemical pollutants during critical developmental period causes adverse consequences later in life. In uterus, perfluorooctanesulfonate (PFOS) exposure has been known to cause developmental neurotoxicity, such as increased motor activity, reduced habitation and impaired cognitive function. The possible mechanism of the impaired cognitive function induced by prenatal PFOS exposure was evaluated in this study. Pregnant Sprague Dawley (SD) rats were given 0.1, 0.6, and 2.0 mg kg−1 birth weight (bw) d−1 by gavage from gestation day (GD) 0 to GD20. Control received 0.5% Tween‐20 vehicle (4 ml kg−1 bw d−1). PFOS concentration in hippocampus of offspring was observed on postnatal day (PND) 0 and PND21. The ultrastructure of hippocampus and the gene expression of synaptic vesicle associated proteins in offspring hippocampus, which were important for the neurotransmitter release, were investigated. The transmission electron photomicrographs of the offspring hippocampus from PFOS‐treated maternal groups showed the ultrastructure of synapses was negatively affected. The offspring from PFOS‐treated maternal groups also differed significantly from controls with respect to the expression of synaptic vesicle associated proteins. The mRNA levels of synapsin1 (Syn1), synapsin2 (Syn2), and synaptophysin (Syp) were decreased in treated groups either on PND0 or on PND21. However, the mRNA level of synapsin3 (Syn3) decreased in 0.6‐ and 2.0‐mg kg−1 group on PND0, and showed no significant difference among control group and all treated groups on PND21. These results indicate that the impairment of cognitive function induced by PFOS may be attributed to the lower mRNA levels of synaptic vesicle associated proteins and the change of synaptic ultrastructure in hippocampus. Synapse, 2010. © 2010 Wiley‐Liss, Inc.