Given the opposing responses reported for bisphenol A (BPA) in terms of induction of obesogenic effects and impaired lipid metabolism, the increasing use of bisphenol F (BPF), and the relatively low information available regarding the effects of bisphenol A bis(3-chloro-2- hydroxypropyl) ether (BADGE·2HCl) in aquatic organisms, this work aims to use the zebrafish liver cell line (ZFL) as an alternative model to characterize the toxicity and the lipid metabolism disruptive potential of the selected compounds in fish. All three bisphenols increased intracellular levels of dihydroceramides and ether-triacylglycerides (ether-TGs), suggestive of inhibited cell growth. However, while BPA and BADGE·2HCl caused an increase of saturated and lower unsaturated TGs, BPF caused oxidative stress and the decrease of TGs containing polyunsaturated fatty acids (PUFAs). Analysis by qPCR highlighted the up-regulation of the lipogenic genes scd and elovl6 by BPA and BPF in line with an increase of lipids containing saturated and monounsaturated FA and a decrease of lipids containing PUFAs. This study shows that BPA, BPF and BADGE·2HCl target lipid homeostasis in ZFL cells through different mechanisms, and highlights the higher lipotoxicity of BADGE·2HCl compared to BPA and BPF.

鉴于报道的双酚A（BPA）在诱导致肥胖作用和脂质代谢受损方面的对立反应，双酚F（BPF）的使用增加以及关于双酚A双（3-氯）的可用信息相对较少-2-羟丙基）醚（BADGE·2HCl）在水生生物中的作用，这项工作旨在使用斑马鱼肝细胞系（ZFL）作为替代模型来表征所选化合物在鱼类中的毒性和脂质代谢破坏潜力。所有这三种双酚均增加了二氢神经酰胺和醚-三酰基甘油酯（醚-TGs）的细胞内水平，表明细胞生长受到抑制。但是，虽然BPA和BADGE·2HCl导致饱和和较低的不饱和TG增加，BPF会引起氧化应激，并降低含多不饱和脂肪酸（PUFA）的TG的含量。qPCR分析突出了脂肪生成基因的上调BPA和BPF对scd和elov16的影响与含有饱和和单不饱和FA的脂质的增加以及含有PUFA的脂质的减少相一致。这项研究表明，BPA，BPF和BADGE·2HCl通过不同的机制靶向ZFL细胞中的脂质稳态，并突显了BADGE·2HCl的脂毒性高于BPA和BPF。