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全氟烷基酸的神经毒性作用:神经行为缺陷及其分子机制。

Neurotoxic effects of perfluoroalkyl acids: Neurobehavioral deficit and its molecular mechanism.

机构信息

Institute for Translational Medicine, Qingdao University, Qing Dao, 266071, China.

Institute of Environment and Health, Jianghan University, Wu Han, 430056, China.

出版信息

Toxicol Lett. 2019 May 1;305:65-72. doi: 10.1016/j.toxlet.2019.01.012. Epub 2019 Jan 31.

Abstract

Perfluoroalkyl acids (PFAAs), as a group of industrial chemicals, are characterized by persistence, long-distance transmission, bioaccumulation and toxicity, and have been recognized as persistent organic pollutants. However, PFAAs and their related products have been used daily and in industrially products over the past several decades, which resulting in ubiquitous presence in various environmental medias, biota and even in human body. Numerous studies have investigated the neurobehavioral deficit and molecular mechanism underlying those effects of PFAAs in the last decades. In the present review, we summarized the neurotoxic effects of some PFAAs, especially perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA). The potential molecular mechanism for PFAAs-induced neurotoxicity are mainly described in the following aspects: calcium homeostasis and its related signal pathway, synaptogenesis and synaptic plasticity, neurotransmitters, as well as the neural cells apoptosis. By concluding the current evidences, we hope to provide a further prospective to assess the association of environmental PFAAs exposure and neurotoxiology outcomes.

摘要

全氟烷基酸(PFAAs)作为一组工业化学品,具有持久性、远距离传输性、生物蓄积性和毒性,已被确认为持久性有机污染物。然而,在过去几十年中,PFAAs 及其相关产品被广泛应用于日常和工业产品中,导致其在各种环境介质、生物群甚至人体中广泛存在。在过去的几十年里,大量研究调查了 PFAAs 的神经行为缺陷和分子机制。在本综述中,我们总结了一些 PFAAs,特别是全氟辛烷磺酸(PFOS)和全氟辛酸(PFOA)的神经毒性作用。PFAAs 诱导的神经毒性的潜在分子机制主要描述在以下几个方面:钙稳态及其相关信号通路、突触发生和突触可塑性、神经递质以及神经细胞凋亡。通过总结当前的证据,我们希望为评估环境 PFAAs 暴露与神经毒理学结果的关系提供进一步的展望。

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