Due to their structural similarities, 6:2 fluorotelomer sulfonic acid (6:2 FTSA) and 6:2 fluorotelomer carboxylic acid (6:2 FTCA) are often used as alternatives to perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA), respectively. With limited health risk data and 6:2 FTSA detection in water and sludge, the toxicity of these chemicals is of growing concern. Here, adult male mice were exposed with 5 mg/kg/day of 6:2 FTCA or 6:2 FTSA for 28 days to investigate their hepatotoxicological effects. In contrast to 6:2 FTCA, 6:2 FTSA was detected at high and very high levels in serum and liver, respectively, demonstrating bioaccumulation potential and slow elimination. Furthermore, 6:2 FTSA induced liver weight increase, inflammation, and necrosis, whereas 6:2 FTCA caused no obvious liver injury, with fewer significantly altered genes detected compared with that of 6:2 FTSA (39 vs. 412). Although PFOA and PFOS commonly activate peroxisome proliferator-activated receptor α (PPARα), 6:2 FTSA induced an increase in PPARγ and related proteins, but not in lipid metabolism-related genes such as PPARα. Our results showed that 6:2 FTCA and 6:2 FTSA exhibited weak and moderate hepatotoxicity, respectively, compared with that reported for legacies PFOA and PFOS.

中文翻译：

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6：2含氟端粒羧酸和6：2含氟端粒磺酸（长链全氟烷基酸的两种氟化替代物）对成年雄性小鼠的比较肝毒性。

由于它们的结构相似性，通常分别使用6：2氟代端基磺酸（6：2 FTSA）和6：2氟代端基羧酸（6：2 FTCA）替代全氟辛烷磺酸（PFOS）和全氟辛酸（PFOA）。 。由于健康风险数据有限，并且在水和污泥中检测到6：2 FTSA，因此这些化学物质的毒性日益引起人们的关注。在这里，成年雄性小鼠接受5 mg / kg /天的6：2 FTCA或6：2 FTSA暴露28天，以研究其肝毒性作用。与6：2 FTCA相比，在血清和肝脏中分别以高和非常高的水平检测到6：2 FTSA，这表明了其潜在的生物蓄积性和缓慢消除作用。此外，6：2 FTSA引起肝脏重量增加，炎症和坏死，而6：2 FTCA并未引起明显的肝损伤，与6：2 FTSA相比，检测到的显着改变的基因更少（39对412）。尽管PFOA和PFOS通常激活过氧化物酶体增殖物激活受体α（PPARα），但6：2 FTSA诱导PPARγ和相关蛋白的增加，但未引起脂质代谢相关基因（例如PPARα）的增加。我们的结果表明，与传统PFOA和PFOS的报道相比，6：2 FTCA和6：2 FTSA分别显示出弱和中度肝毒性。