17ß-HSD converts:
ANDROSTENEDIONE <=> TESTOSTERONE
ESTRONE (E1) <=> ESTRADIOL (E2)
ESTRADIOL (E2) synthesis occurs principally through oxidation of ESTRONE (E1) - and is a reversible reaction;
The ESTRADIOL (E2) / ESTRONE (E1) ratio before menopause is > 1 - after menopause ESTRONE 1 is the predominant estrogen.
Both ESTRADIOL (E2) and ESTRONE (E1) can be metabolized to the biologically weaker ESTRIOL (E3), and to a number of other metabolites - via A-ring (Anti-carcinogenic) metabolic pathways, E.g, 2-HYDROXYESTRONE and its methylated form 2-METHOXYESTRONE or D-ring (potentially carcinogenic) metabolism E.g, 16α- HYDROXYESTRONE.
Tissue enzymes (E.g sulfatases and 17ß-HSDs) originating in bowel bacterial flora and the intestinal mucosa, activate strogens locally to ESTRADIOL (E2) and ESTRONE (E1). Stanczyk F. Estrogens used for replacement therapy in postmenopausal women. Gynecol Endocrinol. 2001;15(suppl 4):17-25.
17ß-HSD pathway directly affected by:
- Lignans
- Enterolactones (lignan precursors) found in E.g.flaxseed inhibit
- Drugs: Cotinine, Danazol, Cyclosporin A, Lithium chloride.