Perfluorobutanesulfonic Acid (PFBS) Induces Fat Accumulation in HepG2 Human Hepatoma.

IF 1.1 4区 环境科学与生态学 Q4 ENVIRONMENTAL SCIENCES Toxicological and Environmental Chemistry Pub Date : 2020-01-01 Epub Date: 2020-08-26 DOI:10.1080/02772248.2020.1808894
Weipeng Qi, John M Clark, Alicia R Timme-Laragy, Yeonhwa Park
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引用次数: 6

Abstract

Per- and poly-fluoroalkyl substances, especially perfluorooctanesulfonic acid, have been extensively used for over 50 years. A growing body of evidence has emerged demonstrating the potential adverse effects of these substances, including its effect on the development of non-alcoholic fatty liver disease, as one of the most prevalent chronic liver diseases. Nonetheless, there is no report of effects of perfluorobutanesulfonic acid, the major replacement for perfluorooctanesulfonic acid, on non-alcoholic fatty liver disease. Therefore, the effects of perfluorobutanesulfonic acid exposure on fat accumulation in a human hepatoma cell line were examined. Cells were exposed to perfluorobutanesulfonic acid with or without 300 μmol/L fatty acid mixture (oleic acid:palmitic acid = 2:1) conjugated by bovine serum albumin as an inducer of steatosis for 48 hours. Perfluorobutanesulfonic acid at 200 μmol/L significantly increased the triglyceride level in the presence of fatty acid compared to the control, but not without fatty acid, which was abolished by a specific peroxisome proliferator-activated receptor gamma antagonist. Perfluorobutanesulfonic acid upregulated key genes controlling lipogenesis and fatty acid uptake. Perfluorobutanesulfonic acid treatment also promoted the production of reactive oxygen species, an endoplasmic reticulum stress marker and cytosolic calcium. In conclusion, perfluorobutanesulfonic acid increased fat accumulation, in part, via peroxisome proliferator-activated receptor gamma-mediated pathway in hepatoma cells.

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全氟丁烷磺酸(PFBS)诱导HepG2人肝癌脂肪堆积。
单氟烷基和多氟烷基物质,特别是全氟辛烷磺酸,已被广泛使用了50多年。越来越多的证据表明这些物质的潜在不利影响,包括其对非酒精性脂肪性肝病发展的影响,非酒精性脂肪性肝病是最普遍的慢性肝病之一。然而,没有关于全氟辛烷磺酸(全氟辛烷磺酸的主要替代品)对非酒精性脂肪肝疾病影响的报告。因此,研究了全氟丁烷磺酸暴露对人肝癌细胞系脂肪积累的影响。将细胞暴露于含或不含300 μmol/L脂肪酸混合物(油酸:棕榈酸= 2:1)的全氟丁烷磺酸中,以牛血清白蛋白偶联脂肪变性诱变剂48小时。与对照组相比,200 μmol/L的全氟丁烷磺酸在有脂肪酸存在的情况下显著提高了甘油三酯水平,但在没有脂肪酸的情况下没有显著提高,这是由一种特异性的过氧化物酶体增殖物激活受体拮抗剂消除的。全氟丁烷磺酸上调了控制脂肪生成和脂肪酸摄取的关键基因。全氟丁烷磺酸处理还促进了活性氧、内质网应激标志物和胞质钙的产生。总之,全氟丁烷磺酸增加了肝癌细胞中的脂肪积累,部分是通过过氧化物酶体增殖物激活受体γ介导的途径。
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来源期刊
Toxicological and Environmental Chemistry
Toxicological and Environmental Chemistry ENVIRONMENTAL SCIENCES-TOXICOLOGY
CiteScore
3.50
自引率
5.60%
发文量
0
期刊介绍: The journal is interdisciplinary in outlook, and manuscripts published in it cover all relevant areas: • inorganic chemistry – trace elements in food and the environment, metal complexes and chelates; • organic chemistry – environmental fate, chemical reactions, metabolites and secondary products, synthesis of standards and labelled materials; • physical chemistry – photochemistry, radiochemistry; • environmental chemistry – sources, fate, and sinks of xenochemicals, environmental partitioning and transport, degradation and deposition; • analytical chemistry – development and optimisation of analytical methods, instrumental and methodological advances, miniaturisation and automation; • biological chemistry – pharmacology and toxicology, uptake, metabolism, disposition of xenochemicals, structure-activity relationships, modes of action, ecotoxicological testing.
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