The role of sex hormones in cancer development is well established and has been cited as a contributing factor in one third of all cancer incidences. Estrogens are known to increase the division of cells in hormone-dependent tissues such as the breast and ovaries.1 It has been suggested that the spatial relationship between the phenolic hydroxyl groups of certain flavonoids is similar to that of estradiol allowing flavonoids to interact with estrogen receptors and to exhibit physiological effects similar to estrogens.47 Because flavonoids share this structural similarity with steroids, retinoids, and thyroid hormones,82 many classes of flavonoids, and particularly isoflavonoids, have been referred to as phytoestrogens. Phy-toestrogens are known to bind estrogen receptors exerting both estrogenic and antiestrogenic effects depending on their concentration, the concentration of endogenous sex hormones present, and the receptor activity of the target tissue involved.
The majority of circulating hormones are bound to sex hormone-binding globulin (SHBG; also known as plasma sex steroid-binding protein, SBP). Free hormones, i.e., hormones not bound to SHBG, are available to migrate into cells and initiate hormonal responses. It is theorized that if there is a decrease in plasma concentrations of SHBG, a decrease in the SHBG rate of metabolism, or an increase in hormone production, there is an associated increase in risk of developing hormone-dependent cancers. Phytoestrogens are known to increase plasma levels of SHBG, thus decreasing the plasma concentration of free estrogen and testosterone. The reduced availability of free androgens and estrogens to the target cells would therefore reduce the risk of hormone-dependent cancers.83 This relationship is based on evidence that high levels of circulating estrogen and low levels of SHBG appear to be associated with increased risk of hormone-dependent cancers involving estrogen such as breast and ovarian cancers.1,83 This relationship also exists for hormone-dependent cancers involving testosterone such as prostate cancer.84
Recent evidence suggests that anthocyanins have weak estrogenic activities relative to other phytoestrogens in the flavonoid and isoflavonoid families. Antho-cyanidins were tested for estrogenic activity in cell culture using an estrogen receptor-positive cell line (MCF-7). The anthocyanidins cyanidin, delphinidin, and pelargonidin (chloride forms) were found to exert estrogenic activity and to bind to estrogen receptor-a to activate estrogen-independent gene expression. Researchers suggested that these compounds may therefore play a role in altering the development of hormone-dependent cancers.85 It was reported that the number of hydroxyl groups had a substantial effect on the estrogenic activity of these compounds. Increasing the number of hydroxyls on the B-ring appeared to reduce receptor affinity. Additionally, researchers concluded that the concentration of anthocyanins required to obtain the observed effects in vivo could be reached through normal dietary consumption.
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