Estriol 3-glucuronide
(Synonyms: 雌三醇3-葡萄糖醛酸苷) 目录号 : GC62961
Estriol-3-glucuronide 存在于正常妊娠羊水中和自然发生的尿液中。
Cas No.:2479-91-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Estriol-3-glucuronide exists in amniotic fluid during normal pregnancy and occurs naturally in urine[1][2].
The present Estriol 3-glucuronide direct RIA has also been used for urine and serum samples[1].
[1]. Sugar J, et al. Estriol-3-glucuronide and estriol-16-glucuronide in amniotic fluid during normal pregnancy. J Clin Endocrinol Metab. 1980;50(1):137-143.
[2]. Ladany S. Isolation of crystalline estriol-3-glucuronide from human pregnancy urine. Steroids. 1968;12(6):717-723.
| Cas No. | 2479-91-6 | SDF | |
| 别名 | 雌三醇3-葡萄糖醛酸苷 | ||
| 分子式 | C24H32O9 | 分子量 | 464.51 |
| 溶解度 | 储存条件 | ||
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.1528 mL | 10.764 mL | 21.5281 mL |
| 5 mM | 0.4306 mL | 2.1528 mL | 4.3056 mL |
| 10 mM | 0.2153 mL | 1.0764 mL | 2.1528 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Preparation of specific antiserum to estradiol 3-glucuronide
J Steroid Biochem 1982 Nov;17(5):511-5.PMID:7176643DOI:10.1016/0022-4731(82)90009-7.
The preparation and antigenic properties of estradiol 3-glucuronide-bovine serum albumin (BSA) conjugate in which the hapten is coupled to the carrier protein through the aminomethyl group at C-6 by glutaraldehyde, have been described. Antibody raised against the immunogen in the rabbit possessed high affinity (Ka = 3.7 x 10(9) M-1) and excellent specificity to estradiol 3-glucuronide, exhibiting no significant cross-reactivities with estrogen glucuronides except for Estriol 3-glucuronide (3.64%) and no cross-reactions with free estrogens, their sulfates and other steroids.
Antigenic properties of estriol 3-glucuronide-[C-6]-bovine serum albumin conjugates having oxime bridges
J Pharmacobiodyn 1983 Sep;6(9):692-7.PMID:6655549DOI:10.1248/bpb1978.6.692.
The preparation and antigenic properties of estriol 3-glucuronide-bovine serum albumin (BSA) conjugate in which the hapten is linked to the carrier protein through an (O-3-carboxypropylcarbamoylmethyl)oxime bridge at the C-6 position on the steroid nucleus, has been described. 16,17-Di-O-acetyl-6-oxoestriol 6-(O-carboxymethyl)oxime 3-glucuronide acetate-methyl ester was condensed with gamma-amino-n-butyric acid by the mixed anhydride method. Subsequent coupling with BSA followed by removal of the protecting groups with alkali gave the desired hapten-BSA conjugate. The antisera elicited in the rabbit with the conjugate were highly specific to Estriol 3-glucuronide, discriminating from other 3-substituted compounds. The specificity of antisera improved by elongation of the 6-(O-carboxymethyl)oxime bridge has been discussed.
ATP-dependent transport of beta-estradiol 17-(beta-D-glucuronide) in rat canalicular membrane vesicles
Am J Physiol 1996 Nov;271(5 Pt 1):G791-8.PMID:8944692DOI:10.1152/ajpgi.1996.271.5.G791.
The ATP-dependent transport of beta-estradiol 17-(beta-D-glucuronide) (E217G), a cholestatic metabolite of estradiol, was investigated in rat liver canalicular membrane vesicles. ATP-dependent transport was dependent on time and temperature and occurred into an osmotically sensitive space; kinetic analysis indicated a saturable transport system (Michaelis-Menten constant value, 75 microM; maximum transport rate, 598 pmol.min-1.mg protein-1). The steroid conjugates estradiol glucuronide, Estriol 3-glucuronide, estriol 16 alpha-glucuronide, testosterone glucuronide, and the three-sulfate conjugate of 17G were effective inhibitors of transport. Bromosulfophthalein, S-(2,4-dinitrophenyl)glutathione, and glutathione disulfide, all substrates of the canalicular ATP-dependent non-bile acid organic anion transport system, were also effective inhibitors, whereas taurocholate had no effect on transport. Conversely, E217G inhibited the ATP-dependent transport of S-(2,4-dinitrophenyl)glutathione. Daunorubicin, vinblastine, etoposide, cyclosporin, and PSC-833, substrates/modulators of P-glycoprotein, were also potent inhibitors of E217G transport, and E217G competitively inhibited the ATP-dependent transport of daunorubicin. C219, a monoclonal antibody against P-glycoprotein, inhibited ATP-dependent transport of E217G and daunorubicin but not of taurocholate or S-(2,4-dinitrophenyl)glutathione. These data indicate that E217G is substrate of both the non-bile acid organic anion transport system and P-glycoprotein but not of the ATP-dependent bile acid transport system in canalicular membranes.
17 beta-estradiol glucuronide: an inducer of cholestasis and a physiological substrate for the multidrug resistance transporter
Cancer Res 1993 Nov 15;53(22):5382-5.PMID:8106146doi
The multidrug resistance (MDR) gene family has been shown to be highly expressed in several normal tissues including the canalicular membrane of the hepatocyte. We report that a cholestatic estrogen metabolite, 17 beta-estradiol glucuronide (E217G), is a substrate for the MDR transporter, P-glycoprotein. In cytotoxicity studies, the MDR sarcoma cell line Dx5 was 4.7-fold resistant to E217G, and the K562/R7 leukemia MDR cell line was 5.0-fold resistant to E217G relative to their parental cell lines. There was also a 2- to 3-fold accumulation defect of [3H]E217G in the MDR cells relative to their parental cell lines. E217G (100 microM) modulated resistance ot doxorubicin, taxol, vinblastine, and etoposide in the Dx5 cells, completely reversing the 30- to 60-fold resistance observed with these agents. E217G had no effect on the toxicity of these compounds in the parental cell line (MES-SA). In contrast, MDR cells were not resistant to the noncholestatic estrogen metabolite, Estriol 3-glucuronide, and this metabolite did not modulate resistance to MDR substrates. ATP-dependent transport of [3H]E217G in rat canalicular membranes was inhibited by several MDR substrates including vinblastine, etoposide, verapamil, cyclosporine, and PSC-833.
A male specific hepatic estrogen binding protein: characteristics and binding properties
Arch Biochem Biophys 1986 Oct;250(1):70-85.PMID:3767382DOI:10.1016/0003-9861(86)90703-4.
Mammalian liver is a sex-steroid responsive tissue in that androgen and estrogen receptors are present and mediate differential hepatic hormonal effects. Further, we and others have found a sexual dimorphism in the hepatic cytosolic content of estrogen binding proteins. In addition to the estrogen receptor, the male has a high-capacity (12.0-15.0 pmol/mg protein) estrogen binding protein (MEB) which demonstrates a moderate affinity for estradiol (Kd = 31.0-43.2 nM) if estradiol metabolizing enzymes are first precipitated with protamine sulfate. This protein exhibits a unique specificity for steroidal estrogens: 2-methoxyestriol greater than estradiol greater than estriol = 2-methoxyestradiol greater than 2-hydroxyestradiol greater than estrone greater than 2-methoxyestrone greater than Estriol 3-glucuronide greater than 2-hydroxyestrone = 3-methoxyestriol greater than androstanediol greater than dihydrotestosterone greater than testosterone. Other androgens such as androstenedione and methyltrienolone, nonsteroidal estrogens such as diethylstilbestrol, and the antiestrogens tamoxifen and 4-hydroxytamoxifen do not compete for [3H]estradiol ([3H]E2) binding. MEB is a relatively small-molecular-weight protein with a Sr of 20.4 A as determined by gel filtration on Sephadex G-100. The kinetics of [3H]E2 association and dissociation at 4 degrees C are very rapid, with t1/2 values of less than 5 s. Sodium molybdate, generally used to stabilize steroid receptors, inhibits MEB-[3H]estradiol binding activity in cytosol in a time- and dose-dependent manner, an effect not observed with partially purified MEB. Magnesium chloride inhibits binding activity of the Sephadex G-100 MEB pool, an effect reversed by EDTA. Other divalent cations also inhibit binding: Mn2+ greater than Mg2+ greater than Ca2+. Furthermore, EDTA complexes of these cations slightly enhance binding relative to EDTA alone: Ca2+ EDTA greater than Mg2+ EDTA greater than Mn2+ EDTA. These results demonstrate that MEB is a unique sex-steroid binding protein, albeit of unknown function, which is distinct from hepatic steroid receptors.