dipalmitoylphosphatidylethanolamine

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 甘油磷脂
• 英文名称: dipalmitoylphosphatidylethanolamine
• 英文别名: 1,2-dipalmitoyl-sn-glycero-3-phosphoethanolamine；DPPE；2-azaniumylethyl [(2S)-2,3-di(hexadecanoyloxy)propyl] phosphate
• 化学式: C₃₇H₇₄NO₈P
• 分子量: 691.97
• InChiKey: SLKDGVPOSSLUAI-DHUJRADRSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  12.5
• 重原子数：
  47
• 可旋转键数：
  39
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.95
• 拓扑面积：
  139
• 氢给体数：
  1
• 氢受体数：
  8

反应信息

• 作为反应物：
  描述：

  dipalmitoylphosphatidylethanolamine 在 sodium cyanoborohydride 作用下， 以 甲醇 、 乙醇 、 氯仿 、 水 为溶剂， 反应 3.0h， 生成 7-hydroxy-7,13-dioxo-10-(palmitoyloxy)-6,8,12-trioxa-3-aza-7η⁵-phosphaoctacosan-1-oic acid
  参考文献：
  名称：

  氨基磷脂连接的美拉德产物的独立合成。

  摘要：

  磷脂连接的糖基化产物应该在体内脂质氧化中起重要作用。报告了磷脂酰乙醇胺（PE）衍生的Amadori化合物4-羟基-4-氧代-1-[[（棕榈酰氧基）甲基] -9-（2,3,4,5-四羟基ytetrahydro- 2H-吡喃-2-基）-3,5-二氧杂-8-氮杂-4lambda5-ph膦酸-1-基棕榈酸酯，吡咯甲醛2-[[[[2- [2-甲酰基-5-（羟甲基）-1H-吡咯-1-基]乙氧基]（羟基）磷基]氧基] -1-[（棕榈酰氧基）甲基]乙基棕榈酸酯，羧甲基（CM）衍生物7-羟基-7,13-二氧代-10-（棕榈酰氧基）- 6,8,12-trioxa-3-aza- + ++ 7lambda5-phosphaoctacosan-1-oic acid和羧乙基（CE）衍生物7-hydroxy-2-methyl-7,13-dioxo-10-（palmitoyloxy） -6,8,12-三氧杂++++ +

  DOI：

  10.1016/s0008-6215(99)00330-4

文献信息

• Bioorthogonal control of the phosphorescence and singlet oxygen photosensitisation properties of iridium(<scp>iii</scp>) tetrazine complexes
  作者：Peter Kam-Keung Leung、Lawrence Cho-Cheung Lee、Herman Ho-Yin Yeung、Kai-Wa Io、Kenneth Kam-Wing Lo

  DOI：10.1039/d1cc00545f

  日期：——

  In this work, we demonstrate bioorthogonal control of the phosphorescence and singlet oxygen photosensitisation properties of new iridium(III) tetrazine complexes by different reaction partners; the system was exploited for organelle-specific staining and modulated photocytotoxic activity applications.

  在这项工作中，我们证明了新的铱（III）四嗪配合物的磷光和单线态氧光敏特性的生物正交控制是通过不同的反应伙伴进行的；该系统被用于细胞器特异性染色和调节光细胞毒性活性的应用。
• TARGETING MICROBUBBLES
  申请人：GRUBBS ROBERT H.

  公开号：US20130123781A1

  公开（公告）日：2013-05-16

  This invention related to manufactured microbubbles, as well as methods of using manufactured microbubbles, for example, in medicinal applications. The invention pertains to the physical structure and materials of the microbubbles, as well as to methods for manufacturing microbubbles, methods for targeting microbubbles for specific medicinal applications, and methods for delivering microbubbles in medical treatment.

  这项发明涉及制造微气泡，以及使用制造的微气泡的方法，例如在医学应用中。该发明涉及微气泡的物理结构和材料，以及制造微气泡的方法，将微气泡定位到特定医学应用的方法，以及在医疗治疗中输送微气泡的方法。
• Remarkable difference of phospholipid molecular chirality in regulating PrP aggregation and cell responses
  作者：Cunli Wang、Xue Wang、Dongdong Wang、Shengxu Qian、Fusheng Zhang、Mingyang Li、Minmin Li、Wenqi Lu、Bo Liu、Guangyan Qing

  DOI：10.1016/j.cclet.2022.03.055

  日期：2023.2

  that molecular chirality of the liposomes dominates conformational transition of PrP106–126 from random coil to β-sheet, binding and adsorption of the monomers and oligomers, and subsequent fibrillation process, resulting in distinct inhibition effect in Ca2+ overload and release, ROS production and cell apoptosis. This work is the first to report that interfacial molecular chirality is a potentially

  朊病毒病是致命的神经退行性疾病，可导致严重的痴呆症。朊病毒肽 (PrP) 106–126的错误折叠和积累至关重要，并且该过程与生物膜密切相关。然而，磷脂膜的分子手性如何影响PrP 106-126聚集尚不清楚。因此，在本研究中，合成了一对l - 和d -天冬氨酸 (Asp) 修饰的 1,2-二棕榈酰-sn-甘油-3-磷酸乙醇胺 (DPPE) 以构建手性脂质体。我们发现l -Asp-DPPE 脂质体强烈抑制 PrP 106-126的寡聚化和淀粉样蛋白生成，无论是作用于单体还是寡聚体，都可以挽救 PrP 106-126诱导的细胞毒性。相比之下，d -Asp-DPPE 脂质体仅在高浓度下抑制肽寡聚化，并且在作用于寡聚体时不能阻止淀粉样蛋白生成，从而导致明显的细胞毒性。细胞凋亡实验、细胞内Ca 2+ ( i Ca 2+ )和内质网(ER)释放Ca 2+的动态变化、活性氧(ROS)的产生、吸附动力学和
• 一对对PrP_106-126聚集有抑制作用的手性磷脂
  申请人：中国科学院大连化学物理研究所

  公开号：CN114369115A

  公开（公告）日：2022-04-19

  本发明公开了一种一对对PrP106‑126聚集有抑制作用的手性氨基酸修饰的磷脂分子,具体应用方式为将手性氨基酸修饰的磷脂分子加工成单层手性磷脂囊泡，与PrP106‑126单体和寡聚体共同孵育，然后使用全功能微孔板检测仪观察PrP106‑126的聚集和纤维化情况。此手性磷脂不仅具有良好的生物相容性，并且对PrP106‑126单体和寡聚体的聚集和纤维化也有显著的抑制效果。
• Covalent Modification of Lipids and Proteins in Rat Hepatocytes and in Vitro by Thioacetamide Metabolites
  作者：Diganta Sarma、Heather Hajovsky、Yakov M. Koen、Nadezhda A. Galeva、Todd D. Williams、Jeffrey L. Staudinger、Robert P. Hanzlik

  DOI：10.1021/tx3001658

  日期：2012.9.17

  Thioacetamide (TA) is a well-known hepatotoxin in rats. Acute doses cause centrilobular necrosis and hyperbilirubinemia while chronic administration leads to biliary hyperplasia and cholangiocarcinoma. Its acute toxicity requires its oxidation to a stable S-oxide (TASO) that is oxidized further to a highly reactive S,S-dioxide (TASO(2)). To explore possible parallels among the metabolism, covalent binding, and toxicity of TA and thiobenzamide (TB), we exposed freshly isolated rat hepatocytes to [C-14]-TASO or [(C2D3)-C-13]-TASO. TLC analysis of the cellular lipids showed a single major spot of radioactivity that mass spectral analysis showed to consist of N-acetimidoyl PE lipids having the same side chain composition as the PE fraction from untreated cells; no carbons or hydrogens from TASO were incorporated into the fatty acyl chains. Many cellular proteins contained N-acetyl- or N-acetimidoyl lysine residues in a 3:1 ratio (details to be reported separately). We also oxidized TASO with hydrogen peroxide in the presence of dipalmitoyl phosphatidylenthanolamine (DPPE) or lysozyme. Lysozyme was covalently modified at five of its six lysine side chains; only acetamide-type adducts were formed. DPPE in liposomes also gave only amide-type adducts, even when the reaction was carried out in tetrahydrofuran with only 10% water added. The exclusive formation of N-acetimidoyl PE in hepatocytes means that the concentration or activity of water must be extremely low in the region where TASO(2) is formed, whereas at least some of the TASO(2) can hydrolyze to acetylsulfinic acid before it reacts with cellular proteins. The requirement for two sequential oxidations to produce a reactive metabolite is unusual, but it is even more unusual that a reactive metabolite would react with water to form a new compound that retains a high degree of chemical reactivity toward biological nucleophiles. The possible contribution of lipid modification to the hepatotoxicity of TA/TASO remains to be determined.