Phthalic acid mono-2-ethylhexyl ester
(Synonyms: 邻苯二甲酸单乙基己基酯,MEHP) 目录号 : GC36902
A metabolite of DEHP and a PPARγ agonist
Cas No.:4376-20-9
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
rac-Mono(ethylhexyl) phthalate (MEHP) is a metabolite of di(2-ethylhexyl) phthalate (DEHP), commonly used as a plasticizer and an identified environmental contaminant, and an agonist of peroxisome proliferator-activated receptor γ (PPARγ).1 It binds to PPARγ when used at concentrations of 50 and 100 ?M and activates PPARγ in a reporter assay using HEK293H cells (EC10 = 1.2 ?M). MEHP (30, 100, and 300 ?M) accumulates in 3T3-L1 adipocytes and increases lipolysis, glucose uptake, and energy metabolism, as well as reduces the size of lipid droplets when used at concentrations of 100 and 300 ?M.2 It also increases the expression of the thermogenesis-related genes Usp1, Cidea, Prdm16, and Trpv1 in 3T3-L1 adipocytes.3 Urinary levels of MEHP in women positively correlate with the risk of unexplained recurrent spontaneous abortion (URSA).4
1.Kratochvil, I., Hofmann, T., Rother, S., et al.Mono(2-ethylhexyl) phthalate (MEHP) and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) but not di(2-ethylhexyl) phthalate (DEHP) bind productively to the peroxisome proliferator-activated receptor γRapid Commun Mass Spectrom.33 Suppl. 1(Suppl. 1)75-85(2019) 2.Chiang, H.-c., Kuo, Y.-T., Shen, C.-C., et al.Mono(2-ethylhexyl)phthalate accumulation disturbs energy metabolism of fat cellsArch. Toxicol.90(3)589-601(2016) 3.Hsu, J.-W., Nien, C.-Y., Yeh, S.-C., et al.Phthalate exposure causes browning-like effects on adipocytes in vitro and in vivoFood Chem. Toxicol.142111487(2020) 4.Aimuzi, R., Huang, S., Luo, K., et al.Levels and health risks of urinary phthalate metabolites and the association between phthalate exposure and unexplained recurrent spontaneous abortion: a large case-control study from ChinaEnviron. Res.212(Pt. C)113393(2022)
| Cas No. | 4376-20-9 | SDF | |
| 别名 | 邻苯二甲酸单乙基己基酯,MEHP | ||
| Canonical SMILES | O=C(O)C1=CC=CC=C1C(OCC(CC)CCCC)=O | ||
| 分子式 | C16H22O4 | 分子量 | 278.34 |
| 溶解度 | Water: 100 mg/mL (359.27 mM); DMSO: ≥ 100 mg/mL (359.27 mM) | 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 | 3.5927 mL | 17.9636 mL | 35.9273 mL |
| 5 mM | 0.7185 mL | 3.5927 mL | 7.1855 mL |
| 10 mM | 0.3593 mL | 1.7964 mL | 3.5927 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。
Organotypic Rat Testicular Organoids for the Study of Testicular Maturation and Toxicology
Front Endocrinol (Lausanne) 2022 Jun 9;13:892342.PMID:35757431DOI:10.3389/fendo.2022.892342.
An in vitro system to study testicular maturation in rats, an important model organism for reproductive toxicity, could serve as a platform for high-throughput drug and toxicity screening in a tissue specific context. In vitro maturation of somatic cells and spermatogonia in organ culture systems has been reported. However, this has been a challenge for organoids derived from dissociated testicular cells. Here, we report generation and maintenance of rat testicular organoids in microwell culture for 28 days. We find that rat organoids can be maintained in vitro only at lower than ambient O2 tension of 15% and organoids cultured at 34°C have higher somatic cell maturation and spermatogonial differentiation potential compared to cultures in 37°C. Upon exposure to known toxicants, Phthalic acid mono-2-ethylhexyl ester and cadmium chloride, the organoids displayed loss of tight-junction protein Claudin 11 and altered transcription levels of somatic cell markers that are consistent with previous reports in animal models. Therefore, the microwell-derived rat testicular organoids described here can serve as a novel platform for the study of testicular cell maturation and reproductive toxicity in vitro.
Vitamin B6 Metabolic Pathway is Involved in the Pathogenesis of Liver Diseases via Multi-Omics Analysis
J Hepatocell Carcinoma 2022 Aug 11;9:729-750.PMID:35979344DOI:10.2147/JHC.S370255.
Purpose: To clarify the underlying regulatory mechanisms of progression from liver cirrhosis to hepatocellular carcinoma (HCC), we analyzed the microbiomics, metabolomics, and proteomics in plasma and tissues from patients with HCC or decompensated liver cirrhosis (DC). Patients and methods: Tissues and plasma from 44 HCC patients and 28 patients with DC were collected for metabolomic analysis. 16S rRNA sequencing was performed in nine HCC tissues (HCCT), four distal noncancerous tissues (HCCN), and 11 DC tissues (DCT). Five HCC tissues had liver cirrhosis (HCCT-LC). Five hepatocellular carcinoma tissues without liver cirrhosis (HCCT-NLC) and five DCT were selected for proteomic sequencing. After combining proteomic and metabolomic analysis, we constructed a mouse model of chronic liver injury using carbon tetrachloride (CCl4) and treated them with vitamin B6 (VB6). Results: 16s rRNA sequence results showed that HCC tissues had higher alpha diversity. The highest LDA scores were detected for Elizabethkingia in HCCT, Subsaxibacter in DCT, and Stenotrophomon in HCCN. Metabolomics results demonstrated some metabolites, including capric acid, L-threonate, choline, alpha-D-Glucose, D-ribose, betaine, 2E-eicosenoic acid, linoleic acid, L-palmitoylcarnitine, taurodeoxycholic acid, L-pyroglutamic acid, androsterone sulfate, and Phthalic acid mono-2-ethylhexyl ester (MEHP), had better diagnostic efficacy than AFP (AUC: 0.852; 95% CI: 0.749, 0.954). In a combined analysis of metabolomics and proteomics, we found that HCCT-LC had more obvious disorders of VB6 metabolism and pentose and glucuronate interconversions than DCT, and kynurenine metabolism disorder was more significant in HCCT-LC than in HCCT-NLC. In the CCl4-induced chronic liver injury model, after VB6 supplementation, inflammatory cell infiltration, hepatocyte edema, and degeneration were significantly improved. Conclusion: We found significant differences in the flora distribution between HCCT and DC; MEHP was a new diagnostic biomarker of HCC, and VB6 ameliorated the inflammatory cell infiltration, hepatocyte edema, and degeneration in chronic liver injury.