State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Jiangsu 210046, China.
Soil and Water Science Department, University of Florida, Gainesville, FL 32611, United States.
Environ Int. 2017 Feb;99:43-54. doi: 10.1016/j.envint.2016.11.014. Epub 2016 Nov 18.
As an emerging persistent organic pollutant (POP), perfluorooctanoate (PFOA) is one of the most abundant perfluorinated compounds (PFCs) in the environment. This review summarized the molecular mechanisms and signaling pathways of PFOA-induced toxicity in animals and humans as well as their implications for health risks in humans. Traditional PFOA-induced signal pathways such as peroxisome proliferating receptor alpha (PPARα), constitutive androstane receptor (CAR), farnesoid X receptor (FXR), and pregnane-X receptor (PXR) may not be important for PFOA-induced health effects on humans. Instead, pathways including p53/mitochondrial pathway, nuclear lipid hyperaccumulation, phosphatidylinositol 3-kinase-serine/threonine protein kinase (PI3K-AKT), and tumor necrosis factor-α/nuclear factor κB (TNF-α/NF-κB) may play an important role for PFOA-induced health risks in humans. Both in vivo and in vitro studies are needed to better understand the PFOA-induced toxicity mechanisms as well as the associated health risk in humans.
作为一种新兴的持久性有机污染物 (POP)，全氟辛烷酸 (PFOA) 是环境中最丰富的全氟化合物 (PFC) 之一。本综述总结了 PFOA 诱导的动物和人类毒性的分子机制和信号通路，以及它们对人类健康风险的影响。传统的 PFOA 诱导信号通路，如过氧化物酶体增殖物激活受体α (PPARα)、组成型雄烷受体 (CAR)、法尼醇 X 受体 (FXR) 和孕烷 X 受体 (PXR)，可能对 PFOA 对人类健康的影响不重要。相反，包括 p53/线粒体途径、核脂质蓄积、磷脂酰肌醇 3-激酶-丝氨酸/苏氨酸蛋白激酶 (PI3K-AKT) 和肿瘤坏死因子-α/核因子 κB (TNF-α/NF-κB) 在内的途径可能在 PFOA 诱导的人类健康风险中发挥重要作用。需要进行体内和体外研究，以更好地了解 PFOA 诱导的毒性机制以及与人类相关的健康风险。
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