Phytoestrogens and Their Human Metabolites Show Distinct Agonistic and Antagonistic Properties on Estrogen Receptor {alpha} (ER{alpha})and ERß in Human Cells

Stefan O. Mueller1, Stephanie Simon, Kun Chae, Manfred Metzler and Kenneth S. Korach

Figure 3 and Table 3 for this article should have run as presented below. The Publisher regrets the error.



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FIG. 3. Transactivational potencies and efficacies of DES, E2, and phytoestrogens in Ishikawa cells stably expressing human ER{alpha} (Ishikawa-hER{alpha}) or ERß (Ishikawa-hERß). Transcriptional activity was measured on reporter vectors containing three copies of (A and B) the consensus ERE (3x ERE) or (C and D) the human C3 promoter. Relative potency was calculated by 100 x EC50 (DES)/EC50 (test compound) and is indicated next to each column. DES was set to 100. EC50 values (ligand concentration yielding half-maximal activation) were derived by nonlinear curve-fitting from transactivation curves obtained in Ishikawa-hER{alpha} or Ishikawa-hERß cells (e.g., Fig. 2) and are given as mean ± standard deviation of at least three independent experiments. Please note (A and C) the logarithmic scale of EC50 values. Relative efficacy was calculated by 100 x efficacy (DES)/efficacy (test compound). DES was set to 100. (B and D) Efficacies (maximum fold induction over control) were determined from transactivation curves obtained in Ishikawa-hER{alpha} or Ishikawa-hERß cells (e.g., Fig. 2) and are given as mean ± standard deviation of at least three independent experiments. *EC50 value could not be determined; therefore, the highest dose tested is given in parentheses.

 

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TABLE 3 Compilation of Characteristic Estrogenic and Antiestrogenic Activitiesa of the Tested Phytoestrogens Compared to DES and E2

 
NOTES

1 To whom correspondence should be addressed at Institute of Toxicology, Merck KGaA, 64271 Darmstadt, Germany. Fax: +49-6151-72 91 8517. E-mail: stefan.o.mueller{at}merck.de.