Herb Source Genista tinctoria Linn. Sophora subprostrata Chun et T. Chen Trifolium pratense Linn
Synonyms 5,7,4'-trihydroxyisoflavone,Prunetol,Sophoricol,Genisteol.
Structural formula:
Molecular Formula and Molecular Weight C15H10O5;270.25
Melting Point 297℃-298℃
Solubility Soluble in DMSO and ethanol,Practically insol in water
Appearance Light Yellow Fine Powder
Claims
Reduces cholesterol and triglyceride levels
Reduces risk of heart disease
Suppresses menopausal symptoms (hot flashes)
Reduces bone breakdown (osteoporosis)
Pharmacology Genistein belongs to the isoflavone class of flavonoids. It is also classified as a phytoestrogen. Phytoestrogens are plant-derived nonsteroidal compounds that possess estrogen-like biological activity. Genistein has been found to have both weak estrogenic and weak anti-estrogenic effects.
Genistein is the aglycone (aglucon) of genistin. The isoflavone is found naturally as the glycoside genistin and as the glycosides 6"-O-malonylgenistin and 6"-O-acetylgenistin. Genistein and its glycosides are mainly found in legumes, such as soybeans and chickpeas. Soybeans and soy foods are the major dietary sources of these substances. Nonfermented soy foods, such as tofu, contain higher levels of the genistein glycosides, while fermented soy foods, such as tempeh and miso, contain higher levels of the aglycone.
Genistein has weak estrogenic activity as measured in in vivo and in vitro assays. In vivo, its estrogenic activity is one-third that of glycitein and four times greater than that of daidzein.
Genistein has been found to have a number of antioxidant activities. It is a scavenger of reactive oxygen species and inhibits lipid peroxidation. It also inhibits superoxide anion generation by the enzyme xanthine oxidase. In addition, genistein, in animal experiments, has been found to increase the activities of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, catalase and glutathione reductase.
Several mechanisms have been proposed for genistein's putative anticarcinogenic activity. These include upregulation of apoptosis, inhibition of angiogenesis, inhibition of DNA topoisomerase II and inhibition of protein tyrosine kinases. Genistein's weak estrogenic activity has been suggested as another mechanism for genistein's putative anti-prostate cancer activity. In addition to the above mechanisms, other mechanisms of genistein's putative anti-prostate cancer activity include inhibition of nuclear factor (NF)-Kappa B in prostate cancer cells, downregulation of TGF (transforming growth factor)-beta and inhibition of EGF (epidermal growth factor)-stimulated growth. Genistein's anti-estrogenic action may be another possible mechanism to explain its putative anti-breast cancer activity. In the final analysis, the mechanism of genistein's putative anticarcinogenic activity is unclear.
The possible anti-atherogenic activity of genistein may be attributed, in part, to its antioxidant activity. Genistein may have some lipid-lowering activity, but the mechanism of this is unclear. The weak estrogenic activity of genistein may also contribute to its possible anti-atherogenic action.
Genistein's weak estrogenic effect may help protect against osteoporosis by preventing bone resorption and promoting increased bone density. Genistein has been found to maintain trabecular bone tissue in rats. However, the mechanism of genistein's possible anti-osteoporotic effect is unclear.
The pharmacokinetics of genistein in humans is complex and not well understood. The major dietary and supplemental form of genistein is the glycoside genistin. Some genistin may be hydrolyzed by hydrochloric acid in the stomach to genistein and some may be hydrolyzed by beta-glucosidases in food to genistein. Most of ingested genistin, however, is delivered to the large intestine intact. In the large intestine, bacterial beta-glucosidases hydrolyze genistin to genistein. Genistein