<13C6>ascorbic acid

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 二氢呋喃
• 英文名称: <13C6>ascorbic acid
• 英文别名: [U-¹³C]-L-ascorbic acid；L-Ascorbic Acid-13C6；(2R)-2-[(1S)-1,2-dihydroxy(1,2-13C2)ethyl]-3,4-dihydroxy-(2,3,4,5-13C4)2H-furan-5-one
• 化学式: C₆H₈O₆
• 分子量: 182.06
• InChiKey: CIWBSHSKHKDKBQ-RQFYRPEFSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -1.6
• 重原子数：
  12
• 可旋转键数：
  2
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.5
• 拓扑面积：
  107
• 氢给体数：
  4
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  <13C6>ascorbic acid 、 丙烯醛 以 水 为溶剂， 反应 2.0h， 生成
  参考文献：
  名称：

  丙烯醛的维生素 C 缀合物的形成及其对氧磷酶介导的转化为 5,6,7,8-四羟基-4-氧代辛醛

  摘要：

  据报道，维生素 C（抗坏血酸）参与体外迈克尔加成反应，与 α,β-不饱和醛（如丙烯醛）形成维生素 C 缀合物。该研究显示了丙烯醛维生素 C 结合物 (AscACR) 在暴露于丙烯醛二乙酸酯的培养的人类单核细胞 THP-1 细胞中形成和代谢的证据。通过使用18 O 和13C 标记与液相色谱-串联质谱法相结合，显示 AscACR 将抗坏血酸内酯水解转化为中间体羧酸。随后羧酸的脱羧产生 5,6,7,8-四羟基-4-氧代辛醛 (THO)。当 THP-1 细胞用抗坏血酸 (1 mM, 18 h) 预处理，然后暴露于二乙酸丙烯醛时，在细胞裂解物和培养基中检测到 THO 作为其五氟苄基肟衍生物。THO形成需要用抗坏血酸和丙烯醛二乙酸酯处理THP-1细胞。内酯酶、人重组对氧磷酶 1 和 2 促进了 AscACR 形成 THO。THP-1 细胞表现出 PON 活性，这解释了 AscACR 在这些细胞中催化转化为

  DOI：

  10.1021/tx900452j

文献信息

• Variation in ascorbic acid oxidation routes in hydrogen peroxide and cupric ion solution as determined by GC/MS
  作者：John C. Deutsch、C. R. Santhosh-Kumar、Kathryn L. Hassell、J. Fred. Kolhouse

  DOI：10.1021/ac00075a006

  日期：1994.2.1

  Recent reports have suggested that ascorbic acid protects low-density lipoprotein from peroxide-induced oxidation, but does not protect and may actually function as a prooxidant in the presence of cupric ions. However, dehydroascorbic acid, (the first oxidation product of ascorbic acid) has been shown to protect low-density lipoprotein from cupric ion oxidation but not peroxide-induced oxidation. We have examined the degradation of ascorbic acid, uniformly labeled [C-13(6)]ascorbic acid, and [6,6-H-2(2)]ascorbic acid in hydrogen peroxide and cupric ion solutions using gas chromatography/mass spectrometry to determine products and routes of oxidation using different oxidant sources. We have found that hydrogen peroxide leads to the formation of a six-carbon product with a mass increment of 32 (a double oxygen addition) relative to ascorbic acid, consistent with the oxidation sequence of ascorbic acid(mass 176) going to dehydroascorbic acid (mass 174) to 2,3-diketogulonic acid (mass 192) to 2,3-diketo-4,5,5,6-tetrahydroxyhexanoic acid (mass 208). Cupric ion solutions, on the other hand, do not appear to induce significant amounts of 2,3-diketo-4,5,5,6-tetrahydroxyhexanoic acid but rather lead to the formation of a threo-hexa-2,4-dienoic acid lactone (mass 174) as the major six-carbon species. These data suggest that different oxidation stresses lead to solutions containing different ascorbic acid oxidation products. These ascorbic acid-derived species could, in turn, interact differently with other substances in the aqueous environment, including free metal ions and low-density lipoprotein. This may help explain previous reports showing divergent protective effects of ascorbic acid and dehydroascorbic acid on low-density lipoprotein when different oxidation methods are used.
• Formation of a Vitamin C Conjugate of Acrolein and Its Paraoxonase-Mediated Conversion into 5,6,7,8-Tetrahydroxy-4-oxooctanal
  作者：Nicholas G. Kesinger、Brandi L. Langsdorf、Alexandre F. Yokochi、Cristobal L. Miranda、Jan F. Stevens

  DOI：10.1021/tx900452j

  日期：2010.4.19

  intermediate carboxylic acid. Subsequent decarboxylation of the carboxylic acid yielded 5,6,7,8-tetrahydroxy-4-oxooctanal (THO). When THP-1 cells were pretreated with ascorbic acid (1 mM, 18 h) and then exposed to acrolein diacetate, THO was detected as its pentafluorobenzyl oxime derivative in the cell lysates and medium. Treatment of THP-1 cells with both ascorbic acid and acrolein diacetate was required

  据报道，维生素 C（抗坏血酸）参与体外迈克尔加成反应，与 α,β-不饱和醛（如丙烯醛）形成维生素 C 缀合物。该研究显示了丙烯醛维生素 C 结合物 (AscACR) 在暴露于丙烯醛二乙酸酯的培养的人类单核细胞 THP-1 细胞中形成和代谢的证据。通过使用18 O 和13C 标记与液相色谱-串联质谱法相结合，显示 AscACR 将抗坏血酸内酯水解转化为中间体羧酸。随后羧酸的脱羧产生 5,6,7,8-四羟基-4-氧代辛醛 (THO)。当 THP-1 细胞用抗坏血酸 (1 mM, 18 h) 预处理，然后暴露于二乙酸丙烯醛时，在细胞裂解物和培养基中检测到 THO 作为其五氟苄基肟衍生物。THO形成需要用抗坏血酸和丙烯醛二乙酸酯处理THP-1细胞。内酯酶、人重组对氧磷酶 1 和 2 促进了 AscACR 形成 THO。THP-1 细胞表现出 PON 活性，这解释了 AscACR 在这些细胞中催化转化为