PUBLICATION
Bisphenol A and its analogs perturb primitive myelopoiesis and inhibit innate immune cell formation during early developmental stages of zebrafish
- Authors
- Zhang, L., Hong, X., Liu, W., Li, Z., Wang, J., Yan, S., Zha, J.
- ID
- ZDB-PUB-250813-7
- Date
- 2025
- Source
- Environment International 202: 109718109718 (Journal)
- Registered Authors
- Keywords
- BPA analogs, Embryotoxicity, Hematopoiesis, Innate immune cell, Primitive hematopoiesis
- MeSH Terms
-
- Bisphenol A Compounds
- Benzhydryl Compounds*/toxicity
- Cell Differentiation/drug effects
- Embryo, Nonmammalian/drug effects
- Myelopoiesis*/drug effects
- Animals
- Phenols*/toxicity
- Water Pollutants, Chemical*/toxicity
- Zebrafish*/embryology
- Zebrafish*/immunology
- Immunity, Innate*/drug effects
- PubMed
- 40795486 Full text @ Environ. Int.
Citation
Zhang, L., Hong, X., Liu, W., Li, Z., Wang, J., Yan, S., Zha, J. (2025) Bisphenol A and its analogs perturb primitive myelopoiesis and inhibit innate immune cell formation during early developmental stages of zebrafish. Environment International. 202:109718109718.
Abstract
Perinatal exposure to bisphenol A (BPA) promotes the development of inflammatory and immune diseases. Nevertheless, the potential mechanisms of this effect and the developmental immunotoxicity of BPA analogs are unclear. Here, embryonic zebrafish were exposed to a range of concentrations of BPA and its analogs. With the exception of bisphenol AF, all of the tested bisphenols reduced neutrophil or macrophage numbers, with the rank order of bisphenol P (BPP) ≈ bisphenol B (BPB) > bisphenol S > BPA ≈ bisphenol F (BPF) > bisphenol Z ≈ bisphenol AP > bisphenol E. We assessed BPA, BPB, BPF, and BPP and revealed that this effect was attributed to the inhibition of primitive myelopoiesis by restricting the differentiation of hemangioblasts to myeloid progenitor cells. Mechanistically, BPP partially overlapped with BPA, which restricted hemangioblast differentiation by acting on scl, gata2, and gata1, whereas BPA mainly acted on scl and gata1. In contrast, BPB targeted gata2, whereas BPF favored lmo2, causing abnormal hemangioblast differentiation. These results highlight the differential developmental immunotoxic targets and mechanisms of BPA and its analogs. Our findings reveal the modes of bisphenol-mediated developmental immunotoxicity, highlighting their link with hematopoiesis disorders.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping