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1 April 2004 Equol Is a Novel Anti-Androgen that Inhibits Prostate Growth and Hormone Feedback
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Abstract

Equol (7-hydroxy-3[4′hydroxyphenyl]-chroman) is the major metabolite of the phytoestrogen daidzein, one of the main isoflavones found abundantly in soybeans and soy foods. Equol may be an important biologically active molecule based on recent studies demonstrating that equol can modulate reproductive function. In this study, we examined the effects of equol on prostate growth and LH secretion and determined some of the mechanisms by which it might act. Administration of equol to intact male rats for 4–7 days reduced ventral prostate and epididymal weight and increased circulating LH levels. Using binding assays, we determined that equol specifically binds 5α-dihydrotestosterone (DHT), but not testosterone, dehydroepiandrosterone, or estrogen with high affinity. Equol does not bind the prostatic androgen receptor, and has a modest affinity for recombinant estrogen receptor (ER) β, and no affinity for ERα. In castrated male rats treated with DHT, concomitant treatment with equol blocked DHT's trophic effects on the ventral prostate gland growth and inhibitory feedback effects on plasma LH levels without changes in circulating DHT. Therefore, equol can bind circulating DHT and sequester it from the androgen receptor, thus altering growth and physiological hormone responses that are regulated by androgens. These data suggest a novel model to explain equol's biological properties. The significance of equol's ability to specifically bind and sequester DHT from the androgen receptor have important ramifications in health and disease and may indicate a broad and important usage for equol in the treatment of androgen-mediated pathologies.

Trent D. Lund, Daniel J. Munson, Megan E. Haldy, Kenneth D. R. Setchell, Edwin D. Lephart, and Robert J. Handa "Equol Is a Novel Anti-Androgen that Inhibits Prostate Growth and Hormone Feedback," Biology of Reproduction 70(4), 1188-1195, (1 April 2004). https://doi.org/10.1095/biolreprod.103.023713
Received: 27 September 2003; Accepted: 1 December 2003; Published: 1 April 2004
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