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ARS Home » Southeast Area » New Orleans, Louisiana » Southern Regional Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #150529


item Boue, Stephen
item Shih, Betty
item Carter-Wientjes, Carol
item Cleveland, Thomas

Submitted to: Intl Symposium on the Role of Soy in Preventing/Treating Chronic Disease
Publication Type: Abstract Only
Publication Acceptance Date: 6/30/2003
Publication Date: 9/30/2003
Citation: Boue, S.M., Wiese, T.E., Burow, M.E., Carter-Wientjes, C.H., Shih, B.Y., Morlaes, V.S., Cleveland, T.E. Antihormonal effects of the soybean phytoalexin glyceollin. 5th International Symposium on the Role of Soy in Preventing and Treating Chronic Disease, September 21-24, 2003, Orlando, FL.

Interpretive Summary:

Technical Abstract: Soy isoflavones have been well characterized for their estrogenic activities, as well as their effects on human health and disease. The types and amounts of these compounds in soy and other plants are controlled by both constitutive expression and stress-induced biosynthesis. The aim of this study was to identify and characterize unique soy phytochemicals that had not been previously assessed for estrogenic or antiestrogenic activity. Here we describe increased biosynthesis of the isoflavonoid phytoalexin compounds, glyceollins, in soy plants grown under stressed conditions. In contrast to the observed estrogenic effects of coumestrol, daidzein and genistein, we observed a marked antiestrogenic effect of glyceollins on ER signaling, which correlated with a comparable suppression of 17B-estradiol (E2)-induced proliferation in MCF-7 cells. Further evaluation revealed greater antagonism towards ERa than ERB in transiently transfected HEK 293 cells. Competition binding assays revealed a greater affinity of glyceollins for ERa versus ERB that correlated to greater suppression of ERa signaling with higher concentrations of glyceollins. In conclusion, we describe the phytoalexin compounds known as glyceollins, that exhibit unique antagonistic effects on ER in both HEK 293 and MCF-7 cells.