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Estrone sulfate

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This article is about estrone sulfate as a hormone. For its use as a medication, seeEstrone sulfate (medication).

Estrone sulfate
Skeletal formula of estrone sulfate
Space-filling model of the estrone sulfate molecule
Names
IUPAC name
17-Oxoestra-1,3,5(10)-trien-3-yl hydrogen sulfate
Systematic IUPAC name
(3aS,3bR,9bS,11aS)-11a-Methyl-1-oxo-2,3,3a,3b,4,5,9b,10,11,11a-decahydro-1H-cyclopenta[a]phenanthren-7-yl hydrogen sulfate
Other names
E1S; Oestrone sulfate; Estrone 3-sulfate; Estra-1,3,5(10)-trien-17-one 3-sulfate
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.006.888Edit this at Wikidata
EC Number
  • 207-120-4
KEGG
UNII
  • InChI=1S/C18H22O5S/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/h3,5,10,14-16H,2,4,6-9H2,1H3,(H,20,21,22)/t14-,15-,16+,18+/m1/s1
    Key: JKKFKPJIXZFSSB-CBZIJGRNSA-N
  • C[C@]12CC[C@H]3[C@H]([C@@H]1CCC2=O)CCC4=C3C=CC(=C4)OS(=O)(=O)O
Properties
C18H22O5S
Molar mass 350.429 g/mol
Except where otherwise noted, data are given for materials in theirstandard state(at 25 °C [77 °F], 100 kPa).

Estrone sulfate,also known asE1S,E1SO4andestrone 3-sulfate,is anatural,endogenoussteroidand anestrogen esterandconjugate.[1][2][3]

In addition to its role as a natural hormone, estrone sulfate is used as amedication,for instance inmenopausal hormone therapy;for information on estrone sulfate as a medication, see theestrone sulfate (medication)article.

Biological function[edit]

E1S itself is biologically inactive, with less than 1% of therelative binding affinityof estradiol for theERαandERβ.[3][4]However, it can betransformedbysteroid sulfatase,also known as estrogen sulfatase, intoestrone,anestrogen.[5]Simultaneously,estrogen sulfotransferases,includingSULT1A1andSULT1E1,convert estrone to E1S, resulting in anequilibriumbetween the two steroids in various tissues.[1][5]Estrone can also be converted by17β-hydroxysteroid dehydrogenasesinto the morepotentestrogenestradiol.[1]E1S levels are much higher than those of estrone and estradiol, and it is thought to serve as a long-lasting reservoir for estrone andestradiolin the body.[1][6][7]In accordance, E1S has been found totransactivatetheestrogen receptorat physiologically relevant concentrations.[8][9]This was diminished with co-application ofirosustat(STX-64), asteroid sulfatase inhibitor,indicating the importance of transformation of estrone sulfate into estrone in the estrogenicity of E1S.[8][9]

Unlike unconjugated estradiol and estrone, which arelipophiliccompounds, E1S is ananionand ishydrophilic.[10][11][12]As a result of this, whereas estradiol and estrone are able to readily diffuse through thelipid bilayersof cells, E1S is unable to permeate throughcell membranes.[10][11][12]Instead, estrone sulfate is transported into cells in a tissue-specific manner byactive transportviaorganic-anion-transporting polypeptides(OATPs), includingOATP1A2,OATP1B1,OATP1B3,OATP1C1,OATP2B1,OATP3A1,OATP4A1,andOATP4C1,as well as by thesodium-dependent organic anion transporter(SOAT; SLC10A6).[11][12][13][14]

E1S, serving as a precursor and intermediate for estrone and estradiol, may be involved in thepathophysiologyofestrogen-associated diseasesincludingbreast cancer,benign breast disease,endometrial cancer,ovarian cancer,prostate cancer,andcolorectal cancer.[1][15][16]For this reason,enzyme inhibitorsof steroid sulfatase and 17β-hydroxysteroid dehydrogenase and inhibitors of OATPs, which prevent activation of E1S into estrone and estradiol, are of interest in the potential treatment of such conditions.[1][16][15]

Affinities and estrogenic potencies of estrogen esters and ethers at the estrogen receptors
Estrogen Other names RBATooltip Relative binding affinity(%)a REP(%)b
ER ERα ERβ
Estradiol E2 100 100 100
Estradiol 3-sulfate E2S; E2-3S ? 0.02 0.04
Estradiol 3-glucuronide E2-3G ? 0.02 0.09
Estradiol 17β-glucuronide E2-17G ? 0.002 0.0002
Estradiol benzoate EB; Estradiol 3-benzoate 10 1.1 0.52
Estradiol 17β-acetate E2-17A 31–45 24 ?
Estradiol diacetate EDA; Estradiol 3,17β-diacetate ? 0.79 ?
Estradiol propionate EP; Estradiol 17β-propionate 19–26 2.6 ?
Estradiol valerate EV; Estradiol 17β-valerate 2–11 0.04–21 ?
Estradiol cypionate EC; Estradiol 17β-cypionate ?c 4.0 ?
Estradiol palmitate Estradiol 17β-palmitate 0 ? ?
Estradiol stearate Estradiol 17β-stearate 0 ? ?
Estrone E1; 17-Ketoestradiol 11 5.3–38 14
Estrone sulfate E1S; Estrone 3-sulfate 2 0.004 0.002
Estrone glucuronide E1G; Estrone 3-glucuronide ? <0.001 0.0006
Ethinylestradiol EE; 17α-Ethynylestradiol 100 17–150 129
Mestranol EE 3-methyl ether 1 1.3–8.2 0.16
Quinestrol EE 3-cyclopentyl ether ? 0.37 ?
Footnotes:a=Relative binding affinities(RBAs) were determined viain-vitrodisplacement oflabeledestradiolfromestrogen receptors(ERs) generally ofrodentuterinecytosol.Estrogen estersare variablyhydrolyzedinto estrogens in these systems (shorter ester chain length -> greater rate of hydrolysis) and the ER RBAs of the esters decrease strongly when hydrolysis is prevented.b= Relative estrogenic potencies (REPs) were calculated fromhalf-maximal effective concentrations(EC50) that were determined viain-vitroβ‐galactosidase(β-gal) andgreen fluorescent protein(GFP)productionassaysinyeastexpressing humanERαand humanERβ.Bothmammaliancellsand yeast have the capacity to hydrolyze estrogen esters.c= The affinities ofestradiol cypionatefor the ERs are similar to those ofestradiol valerateandestradiol benzoate(figure).Sources:See template page.

Chemistry[edit]

See also:List of estrogens,Estrogen ester,andList of estrogen esters

E1S, also known as estrone 3-sulfate or as estra-1,3,5(10)-trien-17-one 3-sulfate, is anaturally occurringestranesteroidand aderivativeofestrone.[17]It is anestrogen conjugateorester,and is specifically the C3sulfateesterof estrone.[17]Related estrogen conjugates includeestradiol sulfate,estriol sulfate,estrone glucuronide,estradiol glucuronide,andestriol glucuronide,while related steroid conjugates includedehydroepiandrosterone sulfateandpregnenolone sulfate.

ThelogPof E1S is 1.4.[15]

Biochemistry[edit]

Biosynthesis[edit]

E1S is produced viaestrogen sulfotransferasesfrom the peripheralmetabolismof the estrogensestradiolandestrone.[18][19][20]Estrogen sulfotransferases are expressed minimally or not at all in thegonads.[21]In accordance, E1S is not secreted in meaningful amounts from the gonads in humans.[22][18]However, measurable amounts of estrogen sulfates are said to be secreted by the ovaries in any case.[23]

Production rates, secretion rates, clearance rates, and blood levels of major sex hormones
Sex Sex hormone Reproductive
phase 		Blood
production rate 		Gonadal
secretion rate 		Metabolic
clearance rate 		Reference range (serum levels)
SIunits Non-SIunits
Men Androstenedione
–
 2.8 mg/day 1.6 mg/day 2200 L/day 2.8–7.3 nmol/L 80–210 ng/dL
Testosterone
–
 6.5 mg/day 6.2 mg/day 950 L/day 6.9–34.7 nmol/L 200–1000 ng/dL
Estrone
–
 150 μg/day 110 μg/day 2050 L/day 37–250 pmol/L 10–70 pg/mL
Estradiol
–
 60 μg/day 50 μg/day 1600 L/day <37–210 pmol/L 10–57 pg/mL
Estrone sulfate
–
 80 μg/day Insignificant 167 L/day 600–2500 pmol/L 200–900 pg/mL
Women Androstenedione
–
 3.2 mg/day 2.8 mg/day 2000 L/day 3.1–12.2 nmol/L 89–350 ng/dL
Testosterone
–
 190 μg/day 60 μg/day 500 L/day 0.7–2.8 nmol/L 20–81 ng/dL
Estrone Follicular phase 110 μg/day 80 μg/day 2200 L/day 110–400 pmol/L 30–110 pg/mL
Luteal phase 260 μg/day 150 μg/day 2200 L/day 310–660 pmol/L 80–180 pg/mL
Postmenopause 40 μg/day Insignificant 1610 L/day 22–230 pmol/L 6–60 pg/mL
Estradiol Follicular phase 90 μg/day 80 μg/day 1200 L/day <37–360 pmol/L 10–98 pg/mL
Luteal phase 250 μg/day 240 μg/day 1200 L/day 699–1250 pmol/L 190–341 pg/mL
Postmenopause 6 μg/day Insignificant 910 L/day <37–140 pmol/L 10–38 pg/mL
Estrone sulfate Follicular phase 100 μg/day Insignificant 146 L/day 700–3600 pmol/L 250–1300 pg/mL
Luteal phase 180 μg/day Insignificant 146 L/day 1100–7300 pmol/L 400–2600 pg/mL
Progesterone Follicular phase 2 mg/day 1.7 mg/day 2100 L/day 0.3–3 nmol/L 0.1–0.9 ng/mL
Luteal phase 25 mg/day 24 mg/day 2100 L/day 19–45 nmol/L 6–14 ng/mL
Notes and sources
Notes:"Theconcentrationof a steroid in the circulation is determined by the rate at which it is secreted from glands, the rate of metabolism of precursor or prehormones into the steroid, and the rate at which it is extracted by tissues and metabolized. Thesecretion rateof a steroid refers to the total secretion of the compound from a gland per unit time. Secretion rates have been assessed by sampling the venous effluent from a gland over time and subtracting out the arterial and peripheral venous hormone concentration. Themetabolic clearance rateof a steroid is defined as the volume of blood that has been completely cleared of the hormone per unit time. Theproduction rateof a steroid hormone refers to entry into the blood of the compound from all possible sources, including secretion from glands and conversion of prohormones into the steroid of interest. At steady state, the amount of hormone entering the blood from all sources will be equal to the rate at which it is being cleared (metabolic clearance rate) multiplied by blood concentration (production rate = metabolic clearance rate × concentration). If there is little contribution of prohormone metabolism to the circulating pool of steroid, then the production rate will approximate the secretion rate. "Sources:See template.

Distribution[edit]

Whereas free steroids like estradiol arelipophilicand can enter cells viapassive diffusion,steroid conjugates like E1S arehydrophilicand are unable to do so.[24][25]Instead, steroid conjugates requireactive transportviamembrane transport proteinsto enter cells.[24][25]

Studies in animals and humans have had mixed findings on uptake of exogenously administered E1S in normal andtumorousmammary glandtissue.[26][27][28][24][25]This is in contrast to substantial uptake of exogenously administered estradiol and estrone by the mammary glands.[26]Another animal study found that E1S wasn't taken up by theuterusbut was taken up by theliver,where it washydrolyzedinto estrone.[29][26]

Metabolism[edit]

Theelimination half-lifeof E1S is 10 to 12 hours.[3]Itsmetabolic clearance rateis 80 L/day/m2.[3]

Ovarian tumorshave been found to expresssteroid sulfataseand have been found to convert E1S into estradiol.[30][31]This may contribute to the often elevated levels of estradiol observed in women withovarian cancer.[30][31]

The image above contains clickable links
Description:Themetabolic pathwaysinvolved in themetabolismofestradioland othernaturalestrogens(e.g.,estrone,estriol) in humans. In addition to themetabolic transformationsshown in the diagram,conjugation(e.g.,sulfationandglucuronidation) occurs in the case of estradiol andmetabolitesof estradiol that have one or more availablehydroxyl(–OH)groups.Sources:See template page.

Levels[edit]

Estrogen levels withradioimmunoassay(RIA) aroundmid-cycleduring the normalmenstrual cyclein women.[32][33]The vertical dashed line in the center is mid-cycle.

E1S levels have been characterized in humans.[33][34][35]E1S usingradioimmunoassay(RIA) have been reported to be 0.96 ± 0.11 ng/mL in men, 0.96 ± 0.17 ng/mL during thefollicular phasein women, 1.74 ± 0.32 ng/mL during theluteal phasein women, 0.74 ± 0.11 ng/mL in women takingoral contraceptives,0.13 ± 0.03 ng/mL inpostmenopausalwomen, and 2.56 ± 0.47 ng/mL in postmenopausal women onmenopausal hormone therapy.[35]In addition, E1S levels inpregnantwomen were 19 ± 5 ng/mL in the first trimester, 66 ± 31 ng/mL in the second trimester, and 105 ± 22 ng/mL in the third trimester.[35]E1S levels are about 10 to 15 times higher than those of estrone in women.[36]

References[edit]

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Further reading[edit]

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