Benzyl butyl phthalate
(Synonyms: 邻苯二甲酸丁苄酯) 目录号 : GC60636
Benzylbutylphthalate是邻苯二甲酸酯(PAEs)的一员，通过上调Zeb1的表达，可引起血管瘤(HA)细胞的迁移和侵袭。Benzylbutylphthalate激活乳腺癌细胞中的芳香烃受体(AhR)，刺激SPHK1/S1P/S1PR3信号传导，促进转移性乳腺癌干细胞(BCSCs)的形成。
Cas No.:85-68-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Benzyl butyl phthalate, a member of phthalic acid esters (PAEs), can trigger the migration and invasion of hemangioma (HA) cells via upregulation of Zeb1. Benzyl butyl phthalate activates aryl hydrocarbon receptor (AhR) in breast cancer cells to stimulate SPHK1/S1P/S1PR3 signaling and enhances formation of metastasis-initiating breast cancer stem cells (BCSCs)[1][2][3].
Benzyl butyl phthalate (BBP) is commonly added during the manufacturing of plastics to increase flexibility and elasticity[1].Benzyl butyl phthalate induces histone modifications in S1PR3 in side population (SP) cells, but not in non-SP cells[3].
[1]. Sun G, et al. Developmental toxicity and cardiac effects of butyl benzyl phthalate in zebrafish embryos. Aquat Toxicol. 2017;192:165-170. [2]. Cui S, et al. Benzyl butyl phthalate (BBP) triggers the migration and invasion of hemangioma cells via upregulation of Zeb1. Toxicol In Vitro. 2019;60:323-329. [3]. Wang YC, et al. Benzyl butyl phthalate promotes breast cancer stem cell expansion via SPHK1/S1P/S1PR3 signaling. Oncotarget. 2016;7(20):29563-29576.
| Cas No. | 85-68-7 | SDF | |
| 别名 | 邻苯二甲酸丁苄酯 | ||
| Canonical SMILES | O=C(C1=CC=CC=C1C(OCC2=CC=CC=C2)=O)OCCCC | ||
| 分子式 | C19H20O4 | 分子量 | 312.36 |
| 溶解度 | DMSO: 100 mg/mL (320.14 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 | 3.2014 mL | 16.0072 mL | 32.0143 mL |
| 5 mM | 0.6403 mL | 3.2014 mL | 6.4029 mL |
| 10 mM | 0.3201 mL | 1.6007 mL | 3.2014 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。
Benzyl butyl phthalate (BBP) induces lung injury and fibrosis through neutrophil extracellular traps
Environ Pollut 2022 Sep 15;309:119743.PMID:35835272DOI:10.1016/j.envpol.2022.119743.
Benzyl butyl phthalate (BBP) is an extensively used plasticizer that has aroused widespread concern about its potential toxicity. Previous evidences demonstrate that BBP exposure is associated with asthma and impaired lung function. Accumulating data indicates that neutrophil extracellular traps (NETs), a particular manner of neutrophil death, play a vital role in the pathogenesis of respiratory diseases. However, the immunotoxicity effects of BBP in lung injury are unclear. Here, we aimed to investigate the potential impacts of BBP-induced NETs on lung injury and fibrosis. Mice treated with BBP exhibited significant lung injury, with alveolar hemorrhage, lung edema and increased neutrophil infiltration. Meanwhile, BBP promoted extensive neutrophil infiltration in bronchoalveolar lavage fluid and NETs deposition in lung tissues. Moreover, BBP clearly triggered NETs formation in vitro, which was confirmed by net-like structures decorated with myeloperoxidase and citrullinated histone H3. Furthermore, BBP fueled glucose uptake and ROS burst of neutrophils playing essential roles during NETs formation. Additionally, we proved that NETs could promote fibrogenesis in murine lung epithelial cells and observed lung fibrosis remarkably after BBP-induced injury. Taken together, our findings indicated that exposure to BBP could increase the risk for lung injury and fibrosis by disturbing innate immunity via NETs formation.
Benzyl butyl phthalate non-linearly affects rat Leydig cell development during puberty
Toxicol Lett 2019 Oct 10;314:53-62.PMID:31319113DOI:10.1016/j.toxlet.2019.07.016.
Benzyl butyl phthalate (BBP) is a widely used plasticizer and has raised public health concerns. Here, we report the effects of BBP on the testis development during rat puberty. BBP (0, 10, 100 or 1000 mg/kg) was gavaged to 35-day-old male Sprague Dawley rats for 21 days. The serum testosterone levels, Leydig cell number, the expressions of Leydig and Sertoli cell genes and proteins were measured. The in vitro effects on steroidogenesis and gene expression in immature Leydig cells were observed. BBP significantly increased serum testosterone level at 10 mg/kg but lowered its level at 1000 mg/kg without affecting serum luteinizing hormone and follicle-stimulating hormone levels. BBP increased Leydig cell number at all doses but inhibited steroidogenic capacity per Leydig cell at 1000 mg/kg. BBP significantly increased the ratio of phosphos-AKT2 (pAKT2)/AKT2, and phosphos-ERK1/2 (pERK1/2)/ERK1/2 in the testis. Mono-benzyl phthalate (the metabolite of BBP) inhibited steroidogenesis but BBP did not affect androgen production in immature Leydig cells in vitro. In conclusion, BBP non-linearly regulates Leydig cell development by increasing Leydig cell number but inhibiting steroidogenesis.
Benzyl butyl phthalate Induced Early lncRNA H19 Regulation in C3H10T1/2 Stem Cell Line
Chem Res Toxicol 2021 Jan 18;34(1):54-62.PMID:33395283DOI:10.1021/acs.chemrestox.0c00129.
Exposure to endocrine-disrupting chemicals used in plastic manufacturing may contribute to the current obesity and diabetes epidemic. Our previous study demonstrated that Benzyl butyl phthalate (BBP) induced adipogenesis in the C3H10T1/2 stem cell line. Here we investigated if BBP deregulated long noncoding RNA H19 and its downstream pathway and whether BBP plays a role in the insulin signaling pathway during adipocyte diiferentiation. Cells treated with an 8 day BBP regimen showed that H19 expression was decreased at day 2 with 50 μM BBP exposure (p < 0.05). However, no significant changes were observed from day 4 to day 8. Expression of miRNA-103/107, H19 regulated miRNAs, was upregulated at day 2 (p < 0.05) but not from day 4 to day 8. Similarly, expression of the let-7 family members (a, b, c, d, f, and g) was also significantly increased at day 2 (p < 0.05 or p < 0.01), except for let-7e. Both let-7 and miRNA-103/107 are targets of H19 and play roles in insulin signaling. Insulin receptor substrate (IRS)-1, one of the key insulin signal transduction regulators, was significantly downregulated from day 2 to day 8 (p < 0.05). Gene expression of insulin receptor (IR) and IRS-2 were not altered by BBP exposure. The ratio of IRS1/IRS2 was significantly decreased from day 2 to day 8. On day 4, phospho-Akt protein expression was significantly decreased (p < 0.05). In conclusion, BBP exposure may lead to metabolic dysregulation by altering vital epigenetic regulators such as lncRNA H19 and its target microRNAs at an earlier stage, which further regulates insulin signaling.
Benzyl butyl phthalate activates prophage, threatening the stable operation of waste activated sludge anaerobic digestion
Sci Total Environ 2021 May 10;768:144470.PMID:33454470DOI:10.1016/j.scitotenv.2020.144470.
The stable operation of the anaerobic digestion of waste activated sludge (WAS) is threatened by numerous emerging contaminants. Meanwhile, the extensive microplastic pollution increased the environmental exposure risk of plasticizer Benzyl butyl phthalate (BBP), the BBP content has reached a substantial level in WAS. However, the effect of BBP on WAS anaerobic digestion is still unknown. Here we show that high-level BBP brings on anaerobic digestion upset. The presence of 10.0 mg/L BBP (in sludge with 17,640 ± 510 mg/L TSS) led to deferred cell lysis, which was confirmed by the results of continuous parallel factor analysis of dissolved organic matter and the liberation of lactate dehydrogenase. Further, the deferred cell rupture was confirmed associate with prophage activation during WAS anaerobic digestion. Besides solubilization, the hydrolysis, acetogenesis and methanogenesis were also affected by the addition of BBP. The long-term effects of BBP revealed that the dominant microbial structure in anaerobic digester was stable, but the abundance of many functional microorganisms was changed, including short chain fatty acid producers and consumers. This work highlights one of the susceptibility mechanisms for WAS anaerobic digestion processes and provides new perspectives for the comprehensive assessment of emerging contaminant's environmental risks.
Pyrroloquinoline quinone attenuated Benzyl butyl phthalate induced metabolic aberration and a hepatic metabolomic analysis
Biochem Pharmacol 2022 Mar;197:114883.PMID:34971587DOI:10.1016/j.bcp.2021.114883.
Benzyl butyl phthalate (BBP) has recently been implicated as an obesogen. Our recent study demonstrated that BBP can exacerbate high fat diet (HFD) induced diabesity in male mice. Here, we explored if pyrroloquinoline quinone (PQQ), a natural antioxidant andphytochemical, can attenuate metabolic aberrations induced by HFD or HFD-BBPcombination. C57Bl/6 male and female mice were fed either a chow diet (CD) or HFD with or without BBP (3 mg/kg body weight/day)and/or PQQ (20 mg/kg/day)for 16 weeks. The mice's body and tissue weight, fasting blood glucose, glucose and insulin tolerance test, and liver metabolites level weremeasured. In HFD-fed male mice, PQQ significantly attenuated the increased body weight, liver weight, fasting blood glucose, and insulin intolerance under BBP exposure.Even though female mice did show some reversal of metabolic characteristics by PQQ, the response was not similar nor consistent with the male population. Amongthe 14 hepatic metabolites that were significantly altered by HFD compared to CD, only three major metabolites (acetyl-L-carnitine, DL-stachytine, and propionylcarnitine) were decreased. These three were shown to have more reduction under BBP exposure in the presence of HFD whereas with addition of PQQ, these metabolites were restored. Pathway analysis and literature search revealed that these metabolites were negatively associated with obesity and were involved in several pathways including beta-oxidation, oxidative stress, and mitochondrial function. Overall,this finding indicated the potential use of PQQ to restore thewide range of aberrant metabolic effectinduced by an obesogen in the presence of a western diet.