Dehydroepiandrosterone Sulfate (sodium salt)
(Synonyms: 去氢表雄酮硫酸钠,Sodium prasterone sulfate) 目录号 : GC43403
A steroid precursor
Cas No.:1099-87-2
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
Dehydroepiandrosterone sulfate (DHEAS) is a metabolite of dehydroepiandrosterone that is the major secretory product of adrenal glands and is the predominant circulating precursor for active steroid hormones in humans. For example, in the fetoplacental-maternal unit, DHEAS acts as the primary precursor for placental estrogen biosynthesis. A normal circulating concentration of DHEAS is ~10 µM in young adults and is dramatically increased in some adrenocortical disorders.
| Cas No. | 1099-87-2 | SDF | |
| 别名 | 去氢表雄酮硫酸钠,Sodium prasterone sulfate | ||
| Canonical SMILES | O=C1CC[C@@]2([H])[C@]3([H])CC=C4C[C@@H](OS(=O)([O-])=O)CC[C@]4(C)[C@@]3([H])CC[C@@]21C.[Na+] | ||
| 分子式 | C19H27O5S•Na | 分子量 | 390.5 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS (pH 7.2) (1:1): 0.5 mg/ml,Ethanol: 2 mg/ml | 储存条件 | Store at -20°C |
| 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 | 2.5608 mL | 12.8041 mL | 25.6082 mL |
| 5 mM | 0.5122 mL | 2.5608 mL | 5.1216 mL |
| 10 mM | 0.2561 mL | 1.2804 mL | 2.5608 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。
Suppression of serum Dehydroepiandrosterone Sulfate levels by insulin: an evaluation of possible mechanisms
J Clin Endocrinol Metab 1989 Nov;69(5):1040-6.PMID:2529264DOI:10.1210/jcem-69-5-1040.
We previously demonstrated a progressive decline in serum Dehydroepiandrosterone Sulfate (DHEA-S) levels in women during a hyperinsulinemic-euglycemic clamp. To determine whether this fall in serum DHEA-S levels might have been due to insulin-stimulated 1) hydrolysis of DHEA-S to dehydroepiandrosterone (DHEA), 2) conversion of DHEA-S/DHEA to androstenedione, and/or 3) urinary excretion of these steroids, 10 additional men were studied by the hyperinsulinemic-euglycemic clamp technique. Each man received a 0.1 U/kg (0.72 nmol/kg) insulin bolus dose, followed by a 10 mU/kg.min (72 pmol/kg.min) insulin infusion for 4 h. An average insulin level of 12,390 +/- 259 (+/- SE) pmol/L (1,726.8 +/- 36 microU/mL) was achieved; serum glucose was maintained at 5.0 +/- 0.1 mmol/L (90.5 +/- 2.3 mg/dL). During the hyperinsulinemia, serum DHEA-S levels fell progressively and were significantly lower than baseline at 4 and 6 h of study (85.5 +/- 5.9% and 79.1 +/- 3.2% of baseline values, respectively; P less than 0.05). Serum DHEA levels fell concurrently and were significantly lower than baseline at 2, 4, and 6 h of study (66.2 +/- 12.3%, 61.6 +/- 11.2%, and 52.9 +/- 10.2% of baseline values, respectively; P less than 0.05). The percent fall in serum DHEA levels correlated positively with the percent fall in serum DHEA-S levels (r = 0.44; P less than 0.02). Serum androstenedione levels also fell progressively during hyperinsulinemia and were significantly lower than baseline at 2, 4, and 6 h of study (71.5 +/- 4.1%, 71.0 +/- 7.2%, and 48.1 +/- 3.3% of baseline values, respectively; P less than 0.05). No change in serum DHEA-S, DHEA, or androstenedione levels occurred in paired control studies, during which 0.45% saline was infused at rates matched exactly to the rates of the dextrose and insulin infusions during the hyperinsulinemic clamp studies. Despite decreasing serum DHEA-S and DHEA levels during hyperinsulinemia, urinary DHEA-S and DHEA glucuronide excretions were increased by 50% (P less than 0.05) and 86% (P = 0.05), respectively, compared to urinary excretion of these steroids during control studies. In contrast, urinary excretion of unconjugated DHEA was unchanged. Quantitatively, however, increased urinary excretion of conjugated DHEA during hyperinsulinemia accounted for only about 5% of the concomitant fall in serum DHEA-S concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
Inactivation of steroid sulfatase by an active site-directed inhibitor, estrone-3-O-sulfamate
Biochemistry 1995 Sep 12;34(36):11508-14.PMID:7547880DOI:10.1021/bi00036a025.
Steroid sulfatases are responsible for the hydrolysis of 3beta-hydroxy steroid sulfates, such as cholesterol and pregnenolone sulfate, and have an important role in regulating the synthesis of estrogenic steroids, from estrone sulfate and Dehydroepiandrosterone Sulfate, in endocrine-dependent tumors. Although little is known about the mechanism by which the sulfate group is removed from a steroid nucleus, an active site-directed sulfatase inhibitor has been developed. This inhibitor, estrone-3-O-sulfamate (EMATE), was synthesized by treating the sodium salt of estrone with sulfamoyl chloride. This compound inhibited not only estrone sulfatase but also dehydroepiandrosterone sulfatase activity in placental microsomes and in intact MCF-7 breast cancer cells. Pretreatment of MCF-7 cells or placental microsomes with EMATE, followed by extensive washing or dialysis indicated irreversible inhibition. This was confirmed by showing that EMATE inhibited estrone sulfatase activity in placental microsomes in a time-, concentration-, and pH-dependent manner. The enzyme is protected from inactivation by estrone sulfate, which is also consistent with active site-directed inhibition. EMATE is proposed to inactivate estrone sulfatase by irreversible sulfamoylation of the enzyme. Maximum enzyme activity was detected at pH 8.6, and the maximum rate of enzyme inactivation by EMATE also occurred at this pH. The pKa values of the enzymatic reaction and pKa of inactivation were 7.2 and 9.8, providing evidence that two active site residues are being modified by EMATE. As the phenolic pKa of tyrosine (9.7) and the pKa of histidine will allow the roles that (6.8) are similar to the pKa values of inactivation, these amino acid residues may play a role in the catalytic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
Fertaric acid amends bisphenol A-induced toxicity, DNA breakdown, and histopathological changes in the liver, kidney, and testis
World J Hepatol 2022 Mar 27;14(3):535-550.PMID:35582291DOI:10.4254/wjh.v14.i3.535.
Background: Bisphenol A (BPA) is present in many plastic products and food packaging. On the other hand, fertaric acid (FA) is a hydroxycinnamic acid. Aim: To investigate the effect of FA on BPA-related liver, kidney, and testis toxicity, DNA breakdown, and histopathology in male rats. Methods: Thirty male albino rats were divided into five equal groups (6 rats/group): Control, paraffin oil, FA-, BPA-, and FA + BPA-treated groups. The control and paraffin oil groups were administered orally with 1 mL distilled water and 1 mL paraffin oil, respectively. The FA-, BPA-, and FA+ BPA-treated groups were administered orally with FA (45 mg/kg, bw) dissolved in 1 mL distilled water, BPA (4 mg/kg, bw) dissolved in 1 mL paraffin oil, and FA (45 mg/kg, bw) followed by BPA (4 mg/kg, bw), respectively. All these treatments were given once a day for 6 wk. Results: BPA induced a significant decrease in serum alkaline phosphatase, acid phosphatase, sodium, potassium and chloride, testosterone, Dehydroepiandrosterone Sulfate, glucose-6-phosphate dehydrogenase, 3β-hydroxysteroid dehydrogenase, and testis protein levels but a highly significant increase in serum aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transpeptidase, lactate dehydrogenase, bilirubin, urea, creatinine, uric acid, luteinizing hormone, follicle stimulating hormone, sex hormone binding globulin, blood urea nitrogen, and testis cholesterol levels. Also, FA inhibited the degradation of liver, kidney, and testis DNA content. Oral administration of FA to BPA-treated rats restored all the above parameters to normal levels. Conclusion: FA ameliorates BPA-induced liver, kidney, and testis toxicity, DNA breakdown, and histopathological changes.
Na+-taurocholate cotransporting polypeptide (NTCP/SLC10A1) ortholog in the marine skate Leucoraja erinacea is not a physiological bile salt transporter
Am J Physiol Regul Integr Comp Physiol 2017 Apr 1;312(4):R477-R484.PMID:28077388DOI:10.1152/ajpregu.00302.2016.
The Na+-dependent taurocholate cotransporting polypeptide (NTCP/SLC10A1) is a hepatocyte-specific solute carrier, which plays an important role in maintaining bile salt homeostasis in mammals. The absence of a hepatic Na+-dependent bile salt transport system in marine skate and rainbow trout raises a question regarding the function of the Slc10a1 gene in these species. Here, we have characterized the Slc10a1 gene in the marine skate, Leucoraja erinacea The transcript of skate Slc10a1 (skSlc10a1) encodes 319 amino acids and shares 46% identity to human NTCP (hNTCP) with similar topology to mammalian NTCP. SkSlc10a1 mRNA was mostly confined to the brain and testes with minimal expression in the liver. An FXR-bile salt reporter assay indicated that skSlc10a1 transported taurocholic acid (TCA) and scymnol sulfate, but not as effectively as hNTCP. An [3H]TCA uptake assay revealed that skSlc10a1 functioned as a Na+-dependent transporter, but with low affinity for TCA (Km = 92.4 µM) and scymnol sulfate (Ki = 31 µM), compared with hNTCP (TCA, Km = 5.4 µM; Scymnol sulfate, Ki = 3.5 µM). In contrast, the bile salt concentration in skate plasma was 2 µM, similar to levels seen in mammals. Interestingly, skSlc10a1 demonstrated transport activity for the neurosteroids Dehydroepiandrosterone Sulfate and estrone-3-sulfate at physiological concentration, similar to hNTCP. Together, our findings indicate that skSlc10a1 is not a physiological bile salt transporter, providing a molecular explanation for the absence of a hepatic Na+-dependent bile salt uptake system in skate. We speculate that Slc10a1 is a neurosteroid transporter in skate that gained its substrate specificity for bile salts later in vertebrate evolution.
Determination of Sodium Tanshinone IIA Sulfonate in human plasma by LC-MS/MS and its application to a clinical pharmacokinetic study
J Pharm Biomed Anal 2016 Mar 20;121:204-208.PMID:26812478DOI:10.1016/j.jpba.2016.01.026.
An assay based on protein precipitation and liquid chromatography-tandem mass spectrometry (LC-MS/MS) has been developed and validated for the quantitative analysis of Sodium Tanshinone IIA Sulfonate (STS) in human plasma. After the addition of dehydroepiandrosterone-D5-3-sulfate sodium salt (DHEAS-D5) as internal standard (IS) and formic acid, plasma samples were prepared by one-step protein precipitation with a mixture of acetonitrile and methanol. Isocratic mobile phase consisted of 0.4 mmol/L ammonium formate buffer (16 ppm formic acid)/acetonitrile (40/60, v/v) on a XSELECT™ HSS T3 column. Detection was performed on a triple-quadrupole mass spectrometer utilizing an electrospray ionization (ESI) interface operating in positive ion and selected reaction monitoring (SRM) mode with the precursor to product ion transitions m/z 373.3→357.1 for STS and m/z 373.0→97.8 for the IS. Calibration curves of STS in human plasma were linear (r=0.9957-0.9998) over the concentration range of 2-1000 ng/mL with acceptable accuracy and precision. The lower limit of quantification in human plasma was 2 ng/mL. The validated LC-MS/MS method has been successfully applied to a pharmacokinetic study of STS in Chinese healthy male volunteers.