6,7-diethoxy-1-(3,4-diethoxy-benzyl)-2-methyl-isoquinolinium; iodide | 10313-81-2

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 异喹啉及其衍生物
• 英文名称: 6,7-diethoxy-1-(3,4-diethoxy-benzyl)-2-methyl-isoquinolinium; iodide
• 英文别名: Perparin-methojodid；6,7-Diaethoxy-1-(3,4-diaethoxy-benzyl)-2-methyl-isochinolinium; Jodid；1-[(3,4-Diethoxyphenyl)methyl]-6,7-diethoxy-2-methylisoquinolin-2-ium iodide；1-[(3,4-diethoxyphenyl)methyl]-6,7-diethoxy-2-methylisoquinolin-2-ium;iodide
• CAS: 10313-81-2
• 化学式: C₂₅H₃₂NO₄*I
• 分子量: 537.438
• InChiKey: SXXHOOBTBDTOJY-UHFFFAOYSA-M

计算性质

• 辛醇/水分配系数(LogP)：
  1.85
• 重原子数：
  31
• 可旋转键数：
  10
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.4
• 拓扑面积：
  40.8
• 氢给体数：
  0
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  6,7-diethoxy-1-(3,4-diethoxy-benzyl)-2-methyl-isoquinolinium; iodide 在 乙醇 、 铂 作用下， 生成 N-Methyl-3',4',6,7-tetraethoxy-1-benzyl-1,2,3,4-tetrahydroisochinolin
  参考文献：
  名称：

  Bruckner; Kajtar, Acta Chimica Academiae Scientiarum Hungaricae, 1959, vol. 21, p. 417,424

  摘要：

  DOI：
• 作为产物：
  描述：

  乙罂粟碱依沙维林 、 碘甲烷 以 甲醇 、 氯仿 为溶剂， 生成 6,7-diethoxy-1-(3,4-diethoxy-benzyl)-2-methyl-isoquinolinium; iodide
  参考文献：
  名称：

  简单的异喹啉和苄基异喹啉生物碱可作为潜在的抗菌剂，抗疟疾剂，细胞毒性剂和抗HIV剂。

  摘要：

  测试了26种简单异喹啉和21种苄基异喹啉的抗微生物，抗疟疾，细胞毒性和抗HIV活性。一些简单的异喹啉生物碱在每种测定法中均具有显着活性，并且可用作开发潜在化学治疗剂的先导化合物。这些化合物包括13（抗微生物），25、26和42（抗动物），13和25（细胞毒性）以及28和29（抗HIV）。异喹啉或二氢异喹啉鎓类型的季氮原子可能有助于提高前三种活性的效力。相反，发现四氢异喹啉盐和6,7-二羟基异喹啉盐具有抗HIV活性。

  DOI：

  10.1016/s0968-0896(01)00154-7

文献信息

• Effects of L-dopa treatment on methylation in mouse brain: Implications for the side effects of L-dopa
  作者：X.X. Liu、K. Wilson、C.G. Charlton

  DOI：10.1016/s0024-3205(00)00557-9

  日期：2000.4

  The effects of L-dopa on methylation process in the mouse brain were investigated. The study is based on recent findings that methylation may play an important role in Parkinson's disease (PD) and in the actions of L-dopa. The methyl donor, S-adenosylmethionine (SAM) and a product of SAM, methyl beta-carboline, were shown to cause PD-like symptoms, when injected into the brain of animals. Furthermore, large amounts of 3-O-methyl dopa, the methyl product of L-dopa, are produced in PD patients receiving L-dopa treatment, and L-dopa induces methionine adenosyl transferase, the enzyme that produces SAM. The results show that, at 0.5 hr, L-dopa (100 mg/kg) decreased the methyl donor, S-adenosylmethionine (SAM) by 36%, increased its metabolite S-adenosylhomocysteine (SAH) by 89% and increased methylation (SAH/SAM) by about 200%. All parameters returned to control values within 4 hr. But 2, 3 and 4 consecutive injections of L-dopa, given at 45 min intervals, depleted SAM by 60, 64 and 76% and increased SAM/SAH to 818, 896, and 1524%. L-dopa (50, 100 and 200 mg/kg) dose-dependently depleted SAM from 24.9 +/- 1.7 nmol/g to 13.0 +/- 0.8, 14.7 +/- 0.8 and 7.7 +/- 0.7 nmol/g, and increased SAH from 1.88 +/- 0.14 to 3.43 +/- 0.26, 4.22 +/- 0.32 and 6.21 +/- 0.40 nmol/g. Brain L-dopa was increased to 326, 335 and 779%, dopamine to 138, 116 and 217% and SAH/SAM to 354, 392 and 1101%. The data show that L-dopa depletes SAM, and increases methylation 4-5 times more than dopamine, therefore, methylation may play a role in the actions of L-dopa. This and other studies suggest that the high level of utilization of methyl group by L-dopa leads to the induction of enzymes to replenish SAM and to increase the methylation of L-dopa as well as DA. These changes may be involved in the side effects of L-dopa.