Immunotoxic Potential of Bisphenol F Mediated through Lipid Signaling Pathways on Macrophages

Chao Zhao, Zhi Tang, Peisi Xie, Kaili Lin, Arthur Chi Kong Chung, Zongwei Cai*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

24 Citations (Scopus)


As a bisphenol A (BPA) alternative, bisphenol F (BPF) has been detected in various products, such as paper products, personal care products, and food. More importantly, the toxicity of BPF remains underexplored. We reported an integrated method to study the immunotoxic potentials and the underlying mechanisms of BPF on cell apoptosis, macrophage polarization, reactive oxygen species generation, expression and secretion of immune-related cytokines, and reprogramming of lipid signaling. More serious to BPA, BPF induced apoptosis in macrophages. The apoptosis was induced by activating both sphingomyelin-ceramide signaling pathway and oxidative stress, which included intrinsic (bax and caspase-9) and extrinsic apoptotic pathways (tumor necrosis factor receptor 1, caspase-8, and caspase-3). BPF exposure also induced the proinflammatory phenotype of the macrophage. This alternation was shown to be closely correlated with the modulation of biosynthesis and degradation of glycerophospholipids. This study demonstrated novel evidence that BPF as a substituent of BPA induced immunotoxic effects at environmentally relevant concentrations. We also showed that the reprogramming of lipidome plays a key role in the regulation of macrophage polarization and the induction of immunotoxicity of the BPA analogue.

Original languageEnglish
Pages (from-to)11420–11428
Number of pages9
JournalEnvironmental Science and Technology
Issue number19
Publication statusPublished - 1 Oct 2019

Scopus Subject Areas

  • Chemistry(all)
  • Environmental Chemistry


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