Estradiol 3-glucuronide

Estradiol 3-glucuronide (E2-3G), also known as 17β-estradiol 3-(β-D-glucuronide), is a naturally occurring and endogenous estrogen conjugate.[1] It is specifically the C3 glucuronide conjugate of estradiol, the major estrogen in the body.[1] It is formed from estradiol in the liver by UDP-glucuronosyltransferase via attachment of glucuronic acid and is eventually excreted in urine and bile.[2][3] Similarly to estrogen sulfates like estrone sulfate, estrogen glucuronides have much higher water solubility than do unconjugated estrogens like estradiol.[3]

Estradiol 3-glucuronide
Names
IUPAC name
(2S,3S,4S,5R,6S)-3,4,5-Trihydroxy-6-[[(8R,9S,13S,14S,17S)-17-hydroxy-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthren-3-yl]oxy]oxane-2-carboxylic acid
Other names
E2-3G; 17β-Estradiol 3-(β-D-glucuronide); 17β-Hydroxyestra-1,3,5(10)-trien-3-yl β-D-glucopyranosiduronic acid;
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
KEGG
Properties
C24H32O8
Molar mass 448.512 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

Estrogen glucuronides can be deconjugated into the corresponding free estrogens by β-glucuronidase in tissues that express this enzyme, such as the mammary gland.[2] As a result, estrogen glucuronides have estrogenic activity via conversion into estrogens.[2]

Estradiol 3-glucuronide is a positional isomer of estradiol 17β-glucuronide.

Affinities and estrogenic potencies of estrogen esters and ethers at the estrogen receptors
Estrogen Other names RBA (%)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 via in-vitro displacement of labeled estradiol from estrogen receptors (ERs) generally of rodent uterine cytosol. Estrogen esters are variably hydrolyzed into 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 from half-maximal effective concentrations (EC50) that were determined via in-vitro β‐galactosidase (β-gal) and green fluorescent protein (GFP) production assays in yeast expressing human ERα and human ERβ. Both mammalian cells and yeast have the capacity to hydrolyze estrogen esters. c = The affinities of estradiol cypionate for the ERs are similar to those of estradiol valerate and estradiol benzoate (figure). Sources: See template page.

See also

References
  1. http://www.hmdb.ca/metabolites/HMDB0006224
  2. Zhu BT, Conney AH (January 1998). "Functional role of estrogen metabolism in target cells: review and perspectives". Carcinogenesis. 19 (1): 1–27. doi:10.1093/carcin/19.1.1. PMID 9472688.
  3. Kuhl H (2005). "Pharmacology of estrogens and progestogens: influence of different routes of administration" (PDF). Climacteric. 8 Suppl 1: 3–63. doi:10.1080/13697130500148875. PMID 16112947.


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