((S)-2-amino-3-(4-hydroxy-3-nitrophenyl)propanoyl)glycylglycyl-L-phenylalanyl-L-leucine | 95231-17-7

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 英文名称: ((S)-2-amino-3-(4-hydroxy-3-nitrophenyl)propanoyl)glycylglycyl-L-phenylalanyl-L-leucine
• CAS: 95231-17-7
• 化学式: C₂₈H₃₆N₆O₉
• 分子量: 600.629
• InChiKey: VUKXMCNVHOVDSG-ACRUOGEOSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -0.25
• 重原子数：
  43.0
• 可旋转键数：
  16.0
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.39
• 拓扑面积：
  243.09
• 氢给体数：
  7.0
• 氢受体数：
  9.0

反应信息

• 作为产物：
  描述：

  Leu-enkephalin 在 copper(II) choride dihydrate 、 双氧水 、 sodium nitrite 作用下， 反应 0.02h， 生成 ((S)-2-amino-3-(4-hydroxy-3-nitrophenyl)propanoyl)glycylglycyl-L-phenylalanyl-L-leucine
  参考文献：
  名称：

  铜催化酪氨酸硝化

  摘要：

  酪氨酸硝化，经常在硝化应激下的神经退行性疾病中观察到，通常被认为是由一氧化氮和氧气形成二氧化氮或过氧亚硝酸盐的分解化学诱导的。它也可以在过氧化氢和亚硝酸盐存在下通过过氧化物酶或超氧化物歧化酶酶促诱导，形成二氧化氮和/或过氧亚硝酸盐。在这项研究中，铜离子在过氧化氢和亚硝酸盐存在下催化酪氨酸硝化的作用，其化学机制与亚硝酸盐被氧化形成二氧化氮的酶促途径非常相似，通过开发一种微反应器也能够进行研究作为电喷雾电离质谱分析的发射器。确实，发现铜离子和肽-铜离子复合物是优异的芬顿催化剂，甚至优于 Fe(III) 或血红素，用于形成 (•)OH 自由基和/或铜 (II) 键合的 (•)OH 自由基过氧化氢。这些自由基被亚硝酸根阴离子有效清除以形成 (•)NO(2) 和酪氨酸以形成酪氨酸自由基，从而导致多肽中的酪氨酸硝化。我们还表明，铜离子可以催化一氧化氮、氧气和过氧化氢的酪氨酸硝化，因为在存在可扩散和/或铜

  DOI：

  10.1021/ja206980q

文献信息

• Light‐Controlled Tyrosine Nitration of Proteins
  作者：Tengfang Long、Lei Liu、Youqi Tao、Wanli Zhang、Jiale Quan、Jie Zheng、Julian D. Hegemann、Motonari Uesugi、Wenbing Yao、Hong Tian、Huan Wang

  DOI：10.1002/anie.202102287

  日期：2021.6.7

  irradiation, dinitroimidazoles efficiently convert tyrosine residues into 3-nitrotyrosine residues in peptides and proteins with fast kinetics and high chemoselectivity under neutral aqueous buffer conditions. The incorporation of 3-nitrotyrosine residues enhances the thermostability of lasso peptide natural products and endows murine tumor necrosis factor-α with strong immunogenicity to break self-tolerance

  蛋白质的酪氨酸硝化是体内最重要的氧化翻译后修饰之一。其生化和生理研究的一个主要障碍是缺乏有效和化学选择性的蛋白质酪氨酸硝化试剂。在此，我们报告了一种通过使用生物相容性二硝基咪唑试剂进行光控蛋白质酪氨酸硝化的通用策略。在 390 nm 照射下，二硝基咪唑在中性水性缓冲液条件下以快速动力学和高化学选择性将肽和蛋白质中的酪氨酸残基有效转化为 3-硝基酪氨酸残基。3-硝基酪氨酸残基的掺入增强了套索肽天然产物的热稳定性，并赋予鼠肿瘤坏死因子-α强大的免疫原性以打破自身耐受。
• Oxidative and nitrative modifications of enkephalins by human neutrophils: effect of nitroenkephalin on leukocyte functional responses
  作者：Elisabetta Capuozzo、Laura Pecci、Federica Giovannitti、Alessia Baseggio Conrado、Mario Fontana

  DOI：10.1007/s00726-011-1147-0

  日期：2012.8

  Neutrophils play a major role in acute inflammation by generating reactive oxygen/nitrogen species. Opioid peptides, including enkephalins, are present at inflammation sites. Neutrophils contribute to protect against inflammatory pain by releasing opioid peptides. In this investigation, the ability of human polymorphonuclear cells to induce oxidative and nitrative modifications of Leu-enkephalin has been investigated in vitro. Activated human neutrophils mediate the oxidation of Leu-enkephalin resulting in the production of dienkephalin. In the presence of nitrite at concentrations observed during inflammatory and infectious process (10-50 mu M), nitroenkephalin, a nitrated derivative of Leu-enkephalin, is additionally formed. The yield of nitroenkephalin increases with nitrite concentration and is significantly inhibited by the addition of catalase or 4-aminobenzoic acid hydrazide (ABAH), a specific inhibitor of peroxidases. These results suggest that neutrophils induce nitration of Leu-enkephalin by a mechanism that is dependent on myeloperoxidase activity and hydrogen peroxide. Oxidative/nitrative modifications of Leu-enkephalin have been also evidenced when cells were treated with the NO-donor molecule, DEANO. The nitrated enkephalin has been examined for its effect on leukocyte functional responses. The data reveal that nitroenkephalin at micromolar concentrations inhibits superoxide anion generation and degranulation of azurophilic granules of human polymorphonuclear cells. Moreover, nitroenkephalin inhibits spontaneous apoptosis of neutrophils, as evaluated by measuring caspase-3 activity. Collectively, our data indicate that the nitrated enkephalin attenuates neutrophil activation and promotes the short-term survival of these cells, suggesting a possible role of the nitrocompound in the efficiency and resolution of inflammatory processes.