However, only three EDCs from group 1 (BPA, BPAF, and HPTE) and four EDCs from group 2 (Dai, Gen, Kaem, and Coum) induced pS2ERE-mediated activation (Figure 2B, right).
2] # ICI BPA # BPAF # HPTE # 4n-NP Dai * Gen # Kaem * Api Coum # Endo Kep 1-BP Relative Iuc activity (fold change) HepG2-ER[alpha] (pS2 ERE Luc) Control [E.
2] ICI # BPA * BPAF HPTE 4n-NP * Dai Gen Kaem Api Coum Endo Kep 1-BP Relative Iuc activity (fold change) HepG2-ER[beta]/cJun (7x AP-1 Luc) Control [E.
The group 1 EDCs BPA and BPAF significantly induced the endogenous ER[alpha] target genes PR, pS2, GREB1, SPUVE, WISP2, and SDF-1, and HPTE significantly induced all of these genes except SDF-1.
2] # ICI BPA # BPAF # HPTE ** 4n-NP Dai * Gen * Kaem * Api Coum ** Endo Kep 1-BP PS2 (fold change) Ishikawa/vec Ishikawa/ER[alpha] Control [E.
In contrast to our reporter assays, in vitro receptor-binding analysis shows that the ligand binding activity of BPAF and HPTE is three times stronger for ER[alpha] than for ER[beta](Matsushima et al.
That makes BPAF
a "double-edged sword," he contends.
CONCLUSION: BPA and BPAF can function as EDCs by acting as cell type--specific agonists([greater than or equal to] 10 nM) or antagonists ([less than or equal to] 10 nM) for ER[alpha] and ER[beta].
KEY WORDS: BPA, BPAF, ER[alpha], ER[alpha] mutants, ER[beta], ERE, estrogen, zearalenone.
However, the mechanism of action of BPA, BPAF, and Zea involving ER[alpha] and ER[alpha] is not well understood in regard to dose dependence, functionality, tissue selectivity, and rapid action responses.
In the present study, we used three different human cell lines to evaluate dose-and cell-specific estrogenic or antagonistic ERE-mediated responses for ER[alpha] or ER[beta] to BPA, BPAF, and Zea.
2], 1,000 nM BPA, 1,000 nM BPAF, or 1,000 nM Zea for 10 min.