These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Bisphenol AF is a full agonist for the estrogen receptor ERalpha but a highly specific antagonist for ERbeta.
    Author: Matsushima A, Liu X, Okada H, Shimohigashi M, Shimohigashi Y.
    Journal: Environ Health Perspect; 2010 Sep; 118(9):1267-72. PubMed ID: 20427257.
    Abstract:
    BACKGROUND: Bisphenol AF has been acknowledged to be useful for the production of CF3-containing polymers with improved chemical, thermal, and mechanical properties. Because of the lack of adequate toxicity data, bisphenol AF has been nominated for comprehensive toxicological characterization. OBJECTIVES: We aimed to determine the relative preference of bisphenol AF for the human nuclear estrogenic receptors ERalpha and ERbeta and the bisphenol A-specific estrogen-related receptor ERRgamma, and to clarify structural characteristics of receptors that influence bisphenol AF binding. METHODS: We examined receptor-binding activities of bisphenol AF relative to [3H]17beta-estradiol (for ERalpha and ERbeta) and [3H]bisphenol A (for ERRgamma). Functional luciferase reporter gene assays were performed to assess receptor activation in HeLa cells. RESULTS: We found that bisphenol AF strongly and selectively binds to ERs over ERRgamma. Furthermore, bisphenol AF receptor-binding activity was three times stronger for ERbeta [IC50 (median inhibitory concentration) = 18.9 nM] than for ERalpha. When examined using a reporter gene assay, bisphenol AF was a full agonist for ERalpha. In contrast, it was almost completely inactive in stimulating the basal constitutive activity of ERbeta. Surprisingly, bisphenol AF acted as a distinct and strong antagonist against the activity of the endogenous ERbeta agonist 17beta-estradiol. CONCLUSION: Our results suggest that bisphenol AF could function as an endocrine-disrupting chemical by acting as an agonist or antagonist to perturb physiological processes mediated through ERalpha and/or ERbeta.
    [Abstract] [Full Text] [Related] [New Search]