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Molecular mechanisms of PFOA-induced toxicity in animals and humans: Implications for health risks

机译:PFOA诱导的动物和人类毒性的分子机制:对健康风险的影响

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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 (PPAR alpha), 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-alphauclear factor kappa B (TNF-alpha/NF-kappa B) 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. Published by Elsevier Ltd.
机译:作为新兴的持久性有机污染物(POP),全氟辛酸酯(PFOA)是环境中最丰富的全氟化合物(PFC)之一。这篇综述总结了PFOA引起动物和人类毒性的分子机制和信号传导途径,以及它们对人类健康风险的影响。传统的PFOA诱导的信号通路,例如过氧化物酶体增殖受体α(PPAR alpha),组成型雄烷受体(CAR),法呢素X受体(FXR)和孕烷X受体(PXR)对于PFOA诱导的对健康的健康影响可能并不重要人类。相反,这些途径包括p53 /线粒体途径,核脂质过度蓄积,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)可能对PFOA引发的人类健康风险起着重要作用。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相关的人类健康风险。由Elsevier Ltd.发布

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