Estradiol sulfate

Estradiol sulfate
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
CAS Number	481-96-9; 4999-79-5 (sodium);
3D model (JSmol)	Interactive image;
ChEBI	CHEBI:4866;
ChEMBL	ChEMBL1628111;
ChemSpider	59790;
PubChem CID	66416;
UNII	4NKQ3751P6;
	InChI InChI=1S/C18H24O5S/c1-18-9-8-14-13-5-3-12(23-24(20,21)22)10-11(13)2-4-15(14)16(18)6-7-17(18)19/h3,5,10,14-17,19H,2,4,6-9H2,1H3,(H,20,21,22)/t14-,15-,16+,17+,18+/m1/s1 Key: QZIGLSSUDXBTLJ-ZBRFXRBCSA-N;
	SMILES CC12CCC3C(C1CCC2O)CCC4=C3C=CC(=C4)OS(=O)(=O)O;
Properties
Chemical formula	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]

Structural properties of selected estradiol esters
Estrogen	Structure	Ester(s)				Relative mol. weight	Relative E2 content^b	logP^c
Estrogen	Structure	Position(s)	Moiet(ies)	Type	Length^a	Relative mol. weight	Relative E2 content^b	logP^c
Estradiol		–	–	–	–	1.00	1.00	4.0
Estradiol acetate		C3	Ethanoic acid	Straight-chain fatty acid	2	1.15	0.87	2.8–3.9
Estradiol benzoate		C3	Benzenecarboxylic acid	Aromatic fatty acid	– (~4–5)	1.38	0.72	4.5–5.7
Estradiol dipropionate		C3, C17β	Propanoic acid (×2)	Straight-chain fatty acid	3 (×2)	1.41	0.71	4.3
Estradiol valerate		C17β	Pentanoic acid	Straight-chain fatty acid	5	1.31	0.76	5.8–6.0
Estradiol cypionate		C17β	Cyclopentylpropanoic acid	Aromatic fatty acid	– (~6)	1.46	0.69	6.5–7.1
Estradiol benzoate butyrate		C3, C17β	Benzoic acid, butyric acid	Mixed fatty acid	– (~6, 2)	1.64	0.61	5.9
Estradiol enantate		C17β	Heptanoic acid	Straight-chain fatty acid	7	1.41	0.71	7.0
Estradiol dienantate		C3, C17β	Heptanoic acid (×2)	Straight-chain fatty acid	7 (×2)	1.82	0.55	8.1–9.1
Estradiol undecylate		C17β	Undecanoic acid	Straight-chain fatty acid	11	1.62	0.62	9.2
Estradiol stearate		C17β	Octadecanoic acid	Straight-chain fatty acid	18	1.98	0.51	12.2
Estradiol distearate		C3, C17β	Octadecanoic acid (×2)	Straight-chain fatty acid	18 (×2)	2.96	0.34	20.2
Estradiol sulfate		C3	Sulfuric acid	Water-soluble conjugate	–	1.29	0.77	0.3–3.8
Estradiol glucuronide		C17β	Glucuronic acid	Water-soluble conjugate	–	1.65	0.61	2.1–2.7
Estramustine phosphate^d		C3, C17β	Normustine, phosphoric acid	Water-soluble conjugate	–	1.91	0.52	2.9–5.0
Polyestradiol phosphate^e		C3–C17β	Phosphoric acid	Water-soluble conjugate	–	1.23^f	0.81^f	2.9^g
Footnotes: ^a = Length of ester in carbon atoms for straight-chain fatty acids or approximate length of ester in carbon atoms for aromatic fatty acids. ^b = Relative estradiol content by weight (i.e., relative estrogenic potency). ^c = Experimental or predicted octanol/water partition coefficient (i.e., lipophilicity/hydrophobicity). Retrieved from PubChem and DrugBank. ^d = Also known as estradiol normustine phosphate. ^e = Polymer of estradiol phosphate (~13 repeat units). ^f = Relative molecular weight or estradiol content per repeat unit. ^g = logP of repeat unit (i.e., estradiol phosphate). Sources: See individual articles.

References

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.
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.
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.
Jorge R. Pasqualini (17 July 2002). Breast Cancer: Prognosis, Treatment, and Prevention. CRC Press. pp. 195–. ISBN 978-0-203-90924-9.
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.
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.
A. T. Gregoire (13 March 2013). Contraceptive Steroids: Pharmacology and Safety. Springer Science & Business Media. pp. 109–. ISBN 978-1-4613-2241-2.
Marc A. Fritz; Leon Speroff (28 March 2012). Clinical Gynecologic Endocrinology and Infertility. Lippincott Williams & Wilkins. pp. 751–. ISBN 978-1-4511-4847-3.
Christian Lauritzen; John W. W. Studd (22 June 2005). Current Management of the Menopause. CRC Press. pp. 364–. ISBN 978-0-203-48612-2.
Ryan J. Huxtable (11 November 2013). Biochemistry of Sulfur. Springer Science & Business Media. pp. 312–. ISBN 978-1-4757-9438-0.
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 2105742. PMID 17073578.
Runge-Morris MA (1997). "Regulation of expression of the rodent cytosolic sulfotransferases". FASEB J. 11 (2): 109–17. PMID 9039952.
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.

This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.

[KinclPasqualini2013-1] 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.

[O'BrienBruce2009-2] 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.

[WangJames2005-3] 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.

[Pasqualini2002-4] Jorge R. Pasqualini (17 July 2002). Breast Cancer: Prognosis, Treatment, and Prevention. CRC Press. pp. 195–. ISBN 978-0-203-90924-9.

[HumansOrganization2007-5] 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.

[LeclercqToma2012-6] 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.

[Gregoire2013-7] A. T. Gregoire (13 March 2013). Contraceptive Steroids: Pharmacology and Safety. Springer Science & Business Media. pp. 109–. ISBN 978-1-4613-2241-2.

[FritzSperoff2012-8] Marc A. Fritz; Leon Speroff (28 March 2012). Clinical Gynecologic Endocrinology and Infertility. Lippincott Williams & Wilkins. pp. 751–. ISBN 978-1-4511-4847-3.

[LauritzenStudd2005-9] Christian Lauritzen; John W. W. Studd (22 June 2005). Current Management of the Menopause. CRC Press. pp. 364–. ISBN 978-0-203-48612-2.

[Huxtable2013-10] Ryan J. Huxtable (11 November 2013). Biochemistry of Sulfur. Springer Science & Business Media. pp. 312–. ISBN 978-1-4757-9438-0.

[KingGhosh2006-11] 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 2105742. PMID 17073578.

[pmid9039952-12] Runge-Morris MA (1997). "Regulation of expression of the rodent cytosolic sulfotransferases". FASEB J. 11 (2): 109–17. PMID 9039952.

[pmid9055636-13] 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.

Estradiol sulfate

See also

References