Phenol Red sodium salt (Phenolsulfonephthalein sodium salt)
(Synonyms: 酚红钠,Phenolsulfonephthalein sodium salt) 目录号 : GC30235
Phenol Red sodium salt (Phenolsulfonephthalein sodium salt) is used ubiquitously as a pH indicator in tissue culture media ranging from 6.8 (yellow) to 8.2 (red). Phenol red binds to the estrogen receptor of MCF-7 human breast cancer cells.
Cas No.:34487-61-1
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
Cell experiment: | Phenol red is dissolved in 0.1% ethanol. To determine the effect of phenol red on cell proliferation, MCF-7 cells grown for 1 week before experiments in phenol red-free MEM supplemented are harvested and seeded into T-25 flasks (ca. 1.5 x 105 cells per flask). The following day, cells from three flasks are harvested and counted with a Coulter Counter. Then the medium is changed to phenol red- and insulin-free MEM, which contains various concentrations of dextran-coated charcoal-treated calf serum, phenol red (0-300 μM), tamoxifen, hydroxytamoxifen, estradiol, or ethanol vehicle (0.1%), and cell number is monitored as a function of time[1]. Phenol Red sodium salt is dissolved in distilled water as a 10 g/L stock solution[2]. |
References: [1]. Berthois Y, et al. Phenol red in tissue culture media is a weak estrogen: implications concerning the study of estrogen-responsive cells in culture. Proc Natl Acad Sci U S A. 1986 Apr;83(8):2496-500. | |
Phenol Red sodium salt (Phenolsulfonephthalein sodium salt) is used ubiquitously as a pH indicator in tissue culture media ranging from 6.8 (yellow) to 8.2 (red). Phenol red binds to the estrogen receptor of MCF-7 human breast cancer cells.
[1] Y Berthois, et al. Proc Natl Acad Sci U S A. 1986 Apr;83(8):2496-500.
| Cas No. | 34487-61-1 | SDF | |
| 别名 | 酚红钠,Phenolsulfonephthalein sodium salt | ||
| Canonical SMILES | O=S1(OC(C2=CC=C([O-])C=C2)(C3=CC=C(O)C=C3)C4=CC=CC=C41)=O.[Na+] | ||
| 分子式 | C19H13NaO5S | 分子量 | 376.36 |
| 溶解度 | Water : ≥ 100 mg/mL (265.70 mM) | 储存条件 | Store at 4°C, protect from light |
| 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 | 2.657 mL | 13.2852 mL | 26.5703 mL |
| 5 mM | 0.5314 mL | 2.657 mL | 5.3141 mL |
| 10 mM | 0.2657 mL | 1.3285 mL | 2.657 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。
Lipophilic impurities, not phenolsulfonphthalein, account for the estrogenic activity in commercial preparations of phenol red
Previously, we found that Phenol Red, a pH indicator dye commonly used in tissue culture media, had weak estrogenic activity, demonstrable by competitive binding to the estrogen receptor, stimulation of the growth rate of human breast cancer (MCF-7) cells, and elevation of progesterone receptor levels in these cells. We have now examined in more detail the source of this estrogenic activity, present in commercially available preparations of Phenol Red. By high performance liquid chromatography and solvent partitioning, we find that the receptor binding and growth promoting activity does not correspond to the indicator dye itself (phenolsulfonphthalein), but rather to more lipophilic impurities present in these preparations. There are numerous such impurities, many of which show some competitive binding activity, but the major receptor binding activity is accounted for by a single impurity component. Commercial preparations of Phenol Red can be purified by ether extraction of the sodium salt, whereby 95-99% of the lipophilic estrogenic impurities are removed, and the growth stimulating activity towards MCF-7 cells is reduced.
Absorption of phenol red from the human lung
Pulmonary absorption of phenol red was studied in normal subjects. Phenol red was administered by intratracheal injection and its urinary excretion was used as an index of pulmonary absorption. Doses ranging from 3 to 30 mg were given to two subjects and urinary phenol red excretion was found to be rate limited. That this effect occurred in the lung was shown by giving the dye intravenously to one subject. A linear relationship between dose and urinary excretion was then observed. Intratracheal p-aminohippurate did not reduce pulmonary absorption of phenol red in one subject. Pulmonary absorption of phenol red dissolved in 0-9% saline and 0-18% saline was compared in nine subjects. Dye absorption was three times greater when it was given in 0-18% saline. When the saline concentration of phenol red doses was held constant there was a linear relationship between the intratracheal dose and urinary excretion in one subject. These results suggest that phenol red is absorbed from the lung by passive diffusion. They also show the importance of solvent effects when studying pulmonary absorption of a substance.
Effect of surfactants on absorption through membranes V: Concentration-dependent effect of a bile salt (sodium deoxycholate) on absorption of a poorly absorbable drug, phenolsulfonphthalein, in humans
The effect of administration of 600-and 300-mg doses of sodium deoxycholate 1 hr before phenolsulfonphthalein solution is reported. The 600-mg dose caused a decrease in drug bioavailability as measured by the total amount excreted in 24 hr. The 300-mg dose cause and increase in the initial phenolsulfonphthalein absorption rate, suggesting a direct action of the bile salt on membrane permeability. The decrease in absorption upon administration of 600 mg was attributed to micellar entrapment of the drug molecule.
Antagonism of ATP responses at P2X receptor subtypes by the pH indicator dye, Phenol red
1 Many types of culture media contain a pH-sensitive dye. One commonly occurring dye, Phenol red sodium (Na(+)) salt, was tested for blocking activity at rat P2X(1-4) receptors (P2X(1-4)Rs) expressed in Xenopus oocytes. 2 Phenol red Na(+)-salt antagonised adenosine 5'-triphosphate (ATP) responses at P2X(1)R (IC(50), 3 microM) and, at higher concentrations, also blocked P2X(2)R and P2X(3)R. Phenol red Na(+)-salt, purified of lipophilic contaminants, blocked P2X(1)R and P2X(3)R by acting as an insurmountable antagonist. 3 Two lipophilic extracts of Phenol red antagonised ATP responses at P2XRs. Extract A was a potent antagonist at P2X(1)R (IC(50), 1.4 microM), whereas extract B was a potent antagonist at P2X(3)R (IC(50), 4.1 microM). A bisphenolic compound (RS151030) found in these extracts was a potent antagonist at P2X(1)R (IC(50), 0.3 microM) and at P2X(3)R (IC(50), 2.4 microM). 4 Phenolphthalein base was a potent irreversible antagonist at P2X(1)R (IC(50), 1 microM), whereas Phenolphthalein K(+)-salt was 25-fold less potent here. 5 Phenolphthalein base was a reversible antagonist of ATP responses at rat P2X(4)R (IC(50), 26 microM), whereas Phenolphthalein K(+)-salt was inactive. 6 Dimethyl sulphoxide (DMSO), used to dissolve lipophilic extracts, showed pharmacological activity by itself at rat P2X(1)R and P2X(4)R. 7 Thus, Phenol red and related compounds are antagonists at rat P2X(1)R, but are also active at other rat P2XRs. Phenolphthalein base is a newly identified, low potency antagonist of ATP responses at P2X(4)R. Culture media containing these red dyes should be used cautiously in future pharmacological studies of P2XRs. Also, wherever possible, the solvent DMSO should be used with caution.
Intestinal permeability enhancement: efficacy, acute local toxicity, and reversibility
The absorption of the polar drug phenol red was assessed in a rat intestinal perfusion model, in the presence of a variety of potential intestinal permeability enhancers. Both the absorption rate constant KA and the plasma phenol red concentration were measured. Perfusates were also assayed for the presence of lactate dehydrogenase (LDH) and lipid phosphate, as biochemical markers of intestinal wall damage. Histological evaluation of surfactant-perfused intestines was also carried out. The potential permeability enhancers studied were the surfactants sodium dodecyl sulfate (SDS), sodium taurocholate (TC), sodium taurodeoxycholate (TDC), polysorbate-80 (PS-80), and nonylphenoxypolyoxyethylene (NP-POE) with an average polar group size of 10.5 POE units. Among these, SDS and NP-POE-10.5 were the most potent permeability enhancers. The bile salt TDC was a more effective enhancer than the more polar TC. The polar non-ionic surfactant PS-80 was an ineffective enhancer. Phenol red KA and plasma level were generally correlated with biochemical and histological measures of intestinal damage. These observations indicate that permeability enhancement and local damage are closely related sequelae of the interaction of surfactants with the intestinal wall, and suggest that local wall damage may be involved in the mechanism of permeability enhancement. The reversibility of permeability enhancement and acute local damage was assessed for the surfactants TDC and NP-POE-10.5. Enhancement of phenol red permeability was reversed within 1-2 hr of the cessation of enhancer treatment. Biochemical markers of local damage also fell to control values within 1-2 hr of removal of enhancer from the perfusate. Histological evaluation of perfused intestines revealed that morphological damage was reversed within 3 hr. These results demonstrate that surfactant-induced acute intestinal wall damage is rapidly repaired.