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饮食作为全氟和多氟烷基物质(PFAS)毒性的暴露源及介质

Diet as an Exposure Source and Mediator of Per- and Polyfluoroalkyl Substance (PFAS) Toxicity.

作者信息

Roth Katherine, Imran Zunaira, Liu Wanqing, Petriello Michael C

机构信息

Institute of Environmental Health Sciences, Wayne State University, Detroit, MI, United States.

Department of Chemistry, Wayne State University, Detroit, MI, United States.

出版信息

Front Toxicol. 2020 Dec 4;2:601149. doi: 10.3389/ftox.2020.601149. eCollection 2020.

DOI:10.3389/ftox.2020.601149
PMID:35296120
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8915917/
Abstract

Per- and polyfluoroalkyl substances (PFAS) are ubiquitously found in the environment due to their widespread commercial use and high chemical stability. Humans are exposed primarily through ingestion of contaminated water and food and epidemiological studies over the last several decades have shown that PFAS levels are associated with adverse chronic health effects, including cardiometabolic disorders such as hyperlipidemia and non-alcoholic fatty liver disease. Perhaps the most well-established effects, as demonstrated in animal studies and human epidemiological studies, are the metabolic alterations PFAS exposure can lead to, especially on lipid homeostasis and signaling. This altered lipid metabolism has often been linked to conditions such as dyslipidemia, leading to fatty liver disease and steatosis. Western diets enriched in high fat and high cholesterol containing foods may be an important human exposure route of PFAS and may also act as an important modulator of associated toxicities. In fact, the chemical structure of PFAS resemble fatty acids and may activate some of the same signaling cascades critical for endogenous metabolism. In this review we aim to outline known dietary exposure sources of PFAS, describe the detrimental metabolic health effects associated with PFAS exposure, and focus on studies examining emerging interaction of dietary effects with PFAS exposure that further alter the dysregulated metabolic state.

摘要

全氟和多氟烷基物质(PFAS)因其广泛的商业用途和高化学稳定性而在环境中普遍存在。人类主要通过摄入受污染的水和食物接触PFAS,过去几十年的流行病学研究表明,PFAS水平与不良慢性健康影响有关,包括高脂血症和非酒精性脂肪性肝病等心脏代谢紊乱。在动物研究和人类流行病学研究中证明,PFAS暴露可能导致的代谢改变,尤其是对脂质稳态和信号传导的影响,可能是最确凿的影响。这种脂质代谢改变常常与血脂异常等情况有关,进而导致脂肪性肝病和脂肪变性。富含高脂肪和高胆固醇食物的西方饮食可能是人类接触PFAS的重要途径,也可能是相关毒性的重要调节因素。事实上,PFAS的化学结构类似于脂肪酸,可能激活一些对内源代谢至关重要的相同信号级联反应。在这篇综述中,我们旨在概述已知的PFAS饮食暴露来源,描述与PFAS暴露相关的有害代谢健康影响,并重点关注研究饮食效应与PFAS暴露之间新出现的相互作用,这种相互作用会进一步改变失调的代谢状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/8915917/bda0cde0e2ef/ftox-02-601149-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/8915917/0d055baee727/ftox-02-601149-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/8915917/bda0cde0e2ef/ftox-02-601149-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/8915917/0d055baee727/ftox-02-601149-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46c4/8915917/bda0cde0e2ef/ftox-02-601149-g0002.jpg

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