ArticleEnvironment & health (Washington, D.C.)2025
Exploring the Antagonistic Effects of Bisphenols with Nonmonotonic Dose-Response Curves on the Estrogen Receptor.
Article in Environment & health (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- BPM Exposure Induces Pulmonary Dysfunction in Adult Mice and Adverse Intergenerational Pulmonary Effects in Offspring.Environment & health (Washington, D.C.) · 2026Article
- Occurrence Patterns of Bisphenol Analogues in Human Blood, Subcutaneous Fat, and Visceral Fat.Environment & health (Washington, D.C.) · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nonmonotonic dose-response curve (NMDRC) is a prevalent characteristic of endocrine-disrupting chemicals (EDCs) in activating nuclear receptors (NRs), implicating intricate regulatory mechanisms. In this study, the agonistic and antagonistic activities of 11 bisphenols on the estrogen receptor (ER) were screened using MVLN cells. Three distinct dose-response patterns were observed, namely, S-shaped, inverted S-shaped, and bell-shaped profiles, corresponding to the agonistic, antagonistic, and nonmonotonic effects on ERs, respectively. To further explore NMDRC, bisphenol B (BPB) and bisphenol AF (BPAF), as representative compounds, were specifically investigated for their antagonistic effects on ER under high exposure concentrations (10-50 μmol/L). Notably, the successive decline in cell viability suggested a subhealthy cell state upon high-dose chemical treatments, compromising cell response in ER transactivation. Unlike the specific effect induced by an ERα antagonist (4-hydroxytamoxifen, 4OHT), the nonspecific inhibitory effects of BPB and BPAF on ER transactivation were further confirmed with their identical antagonistic curves, with or without E2 cotreatment, due to hydrophobicity-related cellular baseline toxicity. Accordingly, the inhibitory effects on NR transactivation might not necessarily be considered as a specific antagonistic activity. Thus, a more cautious inspection is highly encouraged in screening NR antagonism-centered endocrine-disrupting effects of emerging chemicals by carefully reviewing the specificity of signal reduction or inhibition.
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