Estradiol sulfate

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Estradiol sulfate
Estradiol sulfate.svg
Names
IUPAC name
[(8R,9S,13S,14S,17S)-17-Hydroxy-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthren-3-yl] hydrogen sulfate
Other names
Estra-1,3,5(10)-triene-3,17β-diol 3-sulfate
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
UNII
Properties
C18H24O5S
Molar mass 352.445 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

Estradiol sulfate (E2S), or 17β-estradiol 3-sulfate,[1] is a natural, endogenous steroid and an estrogen ester.[2] E2S itself is biologically inactive,[3] but it can be converted by steroid sulfatase (also called estrogen sulfatase) into estradiol, which is a potent estrogen.[2][4][5] Simultaneously, estrogen sulfotransferases convert estradiol to E2S, resulting in an equilibrium between the two steroids in various tissues.[2][5] Estrone and E2S are the two immediate metabolic sources of estradiol.[6] E2S can also be metabolized into estrone sulfate (E1S), which in turn can be converted into estrone and estradiol.[7] Circulating concentrations of E2S are much lower than those of E1S.[1] High concentrations of E2S are present in breast tissue, and E2S has been implicated in the biology of breast cancer via serving as an active reservoir of estradiol.[2][4]

As the sodium salt, sodium estradiol sulfate, E2S is present as a minor constituent (0.9%) of conjugated equine estrogens (CEEs), or Premarin.[8] It effectively functions as a prodrug to estradiol in this preparation, similarly to E1S. E2S is also formed as a metabolite of estradiol, as well as of estrone and E1S.[9][10] Aside from its presence in CEEs, E2S is not available as a commercial pharmaceutical drug.[11]

Although inactive at steroid hormone receptors, E2S has been found to act as a potent inhibitor of glutathione S-transferase,[12] an enzyme that contributes to the inactivation of estradiol via conversion of it into an estradiol-glutathione conjugate.[13] As such, E2S can indirectly serve as a positive effector of estrogen signaling.[12]

See also[edit]

References[edit]

  1. ^ a b F. A. Kincl; J. R. Pasqualini (22 October 2013). Hormones and the Fetus: Volume 1: Production, Concentration and Metabolism During Pregnancy. Elsevier Science. pp. 39–. ISBN 978-1-4832-8538-2. 
  2. ^ a b c d Peter J. O'Brien; William Robert Bruce (2 December 2009). Endogenous Toxins: Targets for Disease Treatment and Prevention, 2 Volume Set. John Wiley & Sons. pp. 869–. ISBN 978-3-527-32363-0. 
  3. ^ Wang, Li-Quan; James, Margaret O. (2005). "Sulfotransferase 2A1 forms estradiol-17-sulfate and celecoxib switches the dominant product from estradiol-3-sulfate to estradiol-17-sulfate". The Journal of Steroid Biochemistry and Molecular Biology. 96 (5): 367–374. doi:10.1016/j.jsbmb.2005.05.002. ISSN 0960-0760. PMID 16011896. 
  4. ^ a b Jorge R. Pasqualini (17 July 2002). Breast Cancer: Prognosis, Treatment, and Prevention. CRC Press. pp. 195–. ISBN 978-0-203-90924-9. 
  5. ^ a b IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; World Health Organization; International Agency for Research on Cancer (2007). Combined Estrogen-progestogen Contraceptives and Combined Estrogen-progestogen Menopausal Therapy. World Health Organization. pp. 279–. ISBN 978-92-832-1291-1. 
  6. ^ G. Leclercq; S. Toma; R. Paridaens; J. C. Heuson (6 December 2012). Clinical Interest of Steroid Hormone Receptors in Breast Cancer. Springer Science & Business Media. pp. 2105–. ISBN 978-3-642-82188-2. 
  7. ^ A. T. Gregoire (13 March 2013). Contraceptive Steroids: Pharmacology and Safety. Springer Science & Business Media. pp. 109–. ISBN 978-1-4613-2241-2. 
  8. ^ Marc A. Fritz; Leon Speroff (28 March 2012). Clinical Gynecologic Endocrinology and Infertility. Lippincott Williams & Wilkins. pp. 751–. ISBN 978-1-4511-4847-3. 
  9. ^ Christian Lauritzen; John W. W. Studd (22 June 2005). Current Management of the Menopause. CRC Press. pp. 364–. ISBN 978-0-203-48612-2. 
  10. ^ Ryan J. Huxtable (11 November 2013). Biochemistry of Sulfur. Springer Science & Business Media. pp. 312–. ISBN 978-1-4757-9438-0. 
  11. ^ King, Roberta; Ghosh, Anasuya; Wu, Jinfang (2006). "Inhibition of Human Phenol and Estrogen Sulfotransferase by Certain Non-Steroidal Anti-Inflammatory Agents". Current Drug Metabolism. 7 (7): 745–753. doi:10.2174/138920006778520615. ISSN 1389-2002. PMC 2105742Freely accessible. PMID 17073578.  More than one of |pmc= and |PMC= specified (help)
  12. ^ a b Runge-Morris MA (1997). "Regulation of expression of the rodent cytosolic sulfotransferases". FASEB J. 11 (2): 109–17. PMID 9039952. 
  13. ^ Singh D, Pandey RS (1996). "Glutathione-S-transferase in rat ovary: its changes during estrous cycle and increase in its activity by estradiol-17 beta". Indian J. Exp. Biol. 34 (11): 1158–60. PMID 9055636.