<1,3-15N2>-6-aminouracil | 89046-42-4

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 二嗪类
• 英文名称: <1,3-15N2>-6-aminouracil
• 英文别名: 6-amino-(1,3-15N2)1H-pyrimidine-2,4-dione
• CAS: 89046-42-4
• 化学式: C₄H₅N₃O₂
• 分子量: 129.089
• InChiKey: LNDZXOWGUAIUBG-AKZCFXPHSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -1.6
• 重原子数：
  9
• 可旋转键数：
  0
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  84.2
• 氢给体数：
  3
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  <1,3-15N2>-6-aminouracil 在 亚硝酸 作用下， 以90%的产率得到<1,3-15N2>-5-nitroso-6-aminouracil
  参考文献：
  名称：

  Synthesis and E.I.M.S. fragmentation analysis of [1,3-15N2] xanthine and [1,3-15N2] caffeine

  摘要：

  高效液相色谱法和质谱法可用于分离和鉴定患者血浆中咖啡因的所有代谢物。[1,3-15N2]黄嘌呤和[1,3- 15N2]咖啡因的合成对阐明质谱碎片路径和明确测定代谢物，特别是作为人体血浆天然成分存在的尿酸具有重要意义。

  DOI：

  10.1002/jlcr.2580360211
• 作为产物：
  描述：

  尿酸-1,3-15N2 在 乙二胺四乙酸 、 氧化亚氮 作用下， 以 phosphate buffer 为溶剂， 生成 <1,3-15N2>-6-aminouracil
  参考文献：
  名称：

  Inactivation of Nitric Oxide by Uric Acid

  摘要：

  The 1980 identification of nitric oxide (NO) as an endothelial cell-derived relaxing factor resulted in an unprecedented biomedical research of NO and established NO as one of the most important cardiovascular, nervous and immune system regulatory molecule. A reduction in endothelial cell NO levels leading to endothelial dysfunction has been identified as a key pathogenic event preceding the development of hypertension, metabolic syndrome, and cardiovascular disease. The reduction in endothelial NO in cardiovascular disease has been attributed to the action of oxidants that either directly react with NO or uncouple its substrate enzyme. In this report, we demonstrate that uric acid (UA), the most abundant antioxidant in plasma, reacts directly with NO in a rapid irreversible reaction resulting in the formation of 6-aminouracil and depletion of NO. We further show that this reaction occurs preferentially with NO even in the presence of oxidants peroxynitrite and hydrogen peroxide and that the reaction is at least partially blocked by glutathione. This study shows a potential mechanism by which UA may deplete NO and cause endothelial dysfunction, particularly under conditions of oxidative stress in which UA is elevated and intracellular glutathione is depleted.

  DOI：

  10.1080/15257770802257952