α-(4-pyridyl-1-oxide)-N-t-butylnitrone | 66893-81-0

• 物质功能分类: 医药中间体 - 杂环化合物 - 吡啶类化合物
• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吡啶及其衍生物
• 英文名称: α-(4-pyridyl-1-oxide)-N-t-butylnitrone
• 英文别名: α-(4-pyridyl 1-oxide)-N-tert-butyl nitrone；alpha-(4-pyridyl-1-oxide)-N-tert-butyl nitrone；alpha-(4-Pyridyl N-oxide)-N-tert-butylnitrone；N-tert-butyl-1-(1-oxidopyridin-1-ium-4-yl)methanimine oxide
• CAS: 66893-81-0
• 化学式: C₁₀H₁₄N₂O₂
• 分子量: 194.233
• InChiKey: RNRMWTCECDHNQU-XYOKQWHBSA-N

物化性质

• 熔点：
  183-185 °C(lit.)
• 沸点：
  330.68°C (rough estimate)
• 密度：
  1.1444 (rough estimate)
• 溶解度：
  水中的溶解度：10mg/mL，澄清，无色至淡黄色

计算性质

• 辛醇/水分配系数(LogP)：
  -0.2
• 重原子数：
  14
• 可旋转键数：
  2
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.4
• 拓扑面积：
  54.2
• 氢给体数：
  0
• 氢受体数：
  2

安全信息

• 海关编码：
  2933399090
• 安全说明：
  S22,S24/25
• WGK Germany：
  3

反应信息

• 作为反应物：
  描述：

  乙醇-1-13C 、 α-(4-pyridyl-1-oxide)-N-t-butylnitrone 在 sodium azide 、 human liver microsomes 、 甲磺酸去铁敏 作用下， 以 phosphate buffer 为溶剂， 反应 2.33h， 生成 [1-13C]-1-hydroxyethyl radical-α-(4-pyridyl-1-oxide)-N-t-butylnitrone adduct
  参考文献：
  名称：

  Rao, D. N. Ramakrishna; Yang, Ming-Xue; Lasker, Jerome M., Molecular Pharmacology, 1996, vol. 49, # 5, p. 814 - 821

  摘要：

  DOI：
• 作为试剂：
  描述：

  丙烯腈 在 双氧水 、 copper dichloride 、 α-(4-pyridyl-1-oxide)-N-t-butylnitrone 作用下， 生成
  参考文献：
  名称：

  Acrylonitrile Enhances H₂O₂-Mediated DNA Damage via Nitrogen-Centered Radical Formation

  摘要：

  Acrylonitrile (ACN) is widely used as a monomer in the polymer industry. Studies on carcinogenicity in rats exposed to ACN showed increased incidences of tumors including glial cell tumors of central nervous system and increased production of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG) in glial cells. Using a high performance liquid chromatograph equipped with an electrochemical detector, we revealed that ACN enhanced the formation of 8-oxo-dG induced by H2O2 and Cu(II) whereas ACN itself did not cause DNA damage. The enhancing effect of ACN was much more efficient in the double-stranded DNA than that in the single-stranded DNA. Experiments with P-32-labeled DNA revealed that addition of ACN enhanced the site-specific DNA damage at guanines, particularly at 5'-site of the CTG and GGG sequences while H2O2/Cu(II) induced piperidine-labile sites at thymine, cytosine, and guanine residues. An electron spin resonance spectroscopy using alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone showed that a nitrogen-centered radical was generated from ACN in the presence of H2O2 and Cu(II). It is considered that ACN enhances H2O2-mediated DNA damage via nitrogen-centered radical formation. We will discuss the mechanism of the enhancing effect on oxidative DNA damage in relation to expression of ACN carcinogenicity.

  DOI：

  10.1021/tx010081s

文献信息

• Rao, D. N. Ramakrishna; Yang, Ming-Xue; Lasker, Jerome M., Molecular Pharmacology, 1996, vol. 49, # 5, p. 814 - 821
  作者：Rao, D. N. Ramakrishna、Yang, Ming-Xue、Lasker, Jerome M.、Cederbaum, Arthur I.

  DOI：——

  日期：——