PUBLICATION
Chlorinated Polyfluoroalkylether Sulfonic Acids Exhibit Stronger Estrogenic Effects than Perfluorooctane Sulfonate by Activating Nuclear Estrogen Receptor Pathways
- Authors
- Xin, Y., Wan, B., Yu, B., Fan, Y., Chen, ., Guo, L.H.
- ID
- ZDB-PUB-200114-5
- Date
- 2020
- Source
- Environmental science & technology 54(6): 3455-3464 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Estrogens
- Sulfonic Acids
- Fluorocarbons*
- Alkanesulfonic Acids*
- PubMed
- 31927955 Full text @ Env. Sci. Tech.
Citation
Xin, Y., Wan, B., Yu, B., Fan, Y., Chen, ., Guo, L.H. (2020) Chlorinated Polyfluoroalkylether Sulfonic Acids Exhibit Stronger Estrogenic Effects than Perfluorooctane Sulfonate by Activating Nuclear Estrogen Receptor Pathways. Environmental science & technology. 54(6):3455-3464.
Abstract
Chlorinated polyfluoroalkylether sulfonic acids (Cl-PFESAs) have been shown to have potential thyroid hormone (TH) disruption effects. Here, we further investigated their estrogenic effects and underlying mechanisms. In vivo results revealed that exposure of zebrafish to Cl-PFESAs induced disorder of sex hormones during the early embryonic stages, and caused histopathological lesions in the gonads of adult zebrafish relative to control groups. To find out whether the estrogen receptor is the molecular target of Cl-PFESAs, the binding interaction between Cl-PFESAs and ERs were investigated using a series of in vitro assays. We found that all tested chemicals could bind directly to ERs and exhibit relatively weak agonistic activity toward ERs, suggesting that ER-mediated signaling pathway is directly involved in the estrogenic effects of Cl-PFESAs. The internal dose of 8:2 Cl-PFESA was significantly higher than the others, which explained why it obviously displayed an ER agonistic effect despite its weak ER binding affinity. Taken together, these results uncover that in addition to TH disruption effect, Cl-PFESAs might also cause estrogenic effects by activating ER pathways.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping