17ß-HSD converts:
ANDROSTENEDIONE <=> TESTOSTERONE
ESTRONE (E1) <=> ESTRADIOL (E2)
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 E1 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-HSD's) originating in bowel bacterial flora and the intestinal mucosa, activate Estrogens 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.
