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双酚 A 单次暴露会改变成年雄性和雌性小鼠重要神经保护蛋白的水平。

A single exposure to bisphenol A alters the levels of important neuroproteins in adult male and female mice.

机构信息

Department of Environmental Toxicology, Uppsala University, Uppsala, Sweden.

出版信息

Neurotoxicology. 2012 Oct;33(5):1390-5. doi: 10.1016/j.neuro.2012.09.002. Epub 2012 Sep 12.

DOI:10.1016/j.neuro.2012.09.002
PMID:22981971
Abstract

Bisphenol A (BPA) is widely used in polymer products in food and beverage containers, baby bottles, dental sealants and fillings, adhesives, protective coatings, flame retardants, water supply pipes, and compact discs, and is found in the environment and in placental tissue, fetuses and breast milk. We have recently reported that a single neonatal exposure to bisphenol A can induce persistent aberrations in spontaneous behavior, in a dose-dependent manner, and affect the adult response to the cholinergic agent nicotine. Furthermore, other recent reports indicate that pre- and perinatal exposure to bisphenol A can induce neurotoxic effects. The present study indicates that a single neonatal exposure to bisphenol A, on postnatal day 10, during the peak of the brain growth spurt, can alter the adult levels of proteins important for normal brain development (CaMKII and synaptophysin). These alterations are induced in both male and female mice and effects are seen in both hippocampus and cerebral cortex. These results further support our recent study showing that neonatal exposure to bisphenol A can act as a developmental neurotoxicant and the effects are similar to effects seen after a single postnatal exposure to other POPs, such as PBDEs, PCBs and PFCs.

摘要

双酚 A(BPA)广泛用于食品和饮料容器、婴儿奶瓶、牙密封剂和填充物、粘合剂、防护涂料、阻燃剂、给水管和光盘等聚合物产品中,并存在于环境中和胎盘组织、胎儿和母乳中。我们最近报告称,新生儿单次接触双酚 A 会以剂量依赖的方式引起自发行为持续异常,并影响成年对胆碱能药物尼古丁的反应。此外,其他最近的报告表明,产前和围产期接触双酚 A 会引起神经毒性作用。本研究表明,在大脑生长突增高峰期的第 10 天新生儿期单次接触双酚 A 会改变成年期对正常大脑发育重要的蛋白质水平(CaMKII 和突触小体蛋白)。这些变化在雄性和雌性小鼠中均被诱导,并且在海马体和大脑皮层中都能看到影响。这些结果进一步支持了我们最近的研究结果,即新生儿期接触双酚 A 可作为一种发育神经毒物,其影响类似于单次接触其他持久性有机污染物(如 PBDEs、PCBs 和 PFCs)后的影响。

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