S-(1,2-二氯乙烯)谷胱甘肽 | 96614-59-4

• 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
• 中文名称: S-(1,2-二氯乙烯)谷胱甘肽
• 英文名称: (E)-S-(1,2-dichlorovinyl)glutathione
• 英文别名: S-(1,2-dichlorovinyl)glutathione；(2S)-2-amino-5-[[(2R)-1-(carboxymethylamino)-3-[(E)-1,2-dichloroethenyl]sulfanyl-1-oxopropan-2-yl]amino]-5-oxopentanoic acid
• CAS: 96614-59-4
• 化学式: C₁₂H₁₇Cl₂N₃O₆S
• 分子量: 402.255
• InChiKey: IXARYIJEQUJTIZ-KWRIXSAHSA-N

物化性质

• 沸点：
  788.2±60.0 °C(Predicted)
• 密度：
  1.533±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  -2.5
• 重原子数：
  24
• 可旋转键数：
  11
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.5
• 拓扑面积：
  184
• 氢给体数：
  5
• 氢受体数：
  8

反应信息

• 作为产物：
  描述：

  谷胱甘肽 、 三氯乙烯 在 氨 、 sodium 作用下， 生成 S-(1,2-二氯乙烯)谷胱甘肽
  参考文献：
  名称：

  Modulation of hepatic and renal metabolism and toxicity of trichloroethylene and perchloroethylene by alterations in status of cytochrome P450 and glutathione

  摘要：

  The relative importance of metabolism of trichloroethylene (Tri) and perchloroethylene (Perc) by the cytochrome P450 (P450) and glutathione (GSH) conjugation pathways in their acute renal and hepatic toxicity was studied in isolated cells and microsomes from rat kidney and liver after various treatments to modulate P450 activity/expression or GSH status. Inhibitors of P450 stimulated GSH conjugation of Tri and, to a lesser extent, Pere, in both kidney cells and hepatocytes. Pere was a more potent, acute cytotoxic agent in isolated kidney cells than Tri but Perc-induced toxicity was less responsive than Tri-induced toxicity to modulation of P450 status. These observations are consistent with P450-dependent bioactivation being more important for Tri than for Perc. Incubation of isolated rat hepatocytes with Tri produced no acute cytotoxicity in isolated hepatocytes while Perc produced comparable cytotoxicity as in kidney cells. Modulation of P450 status in hepatocytes produced larger changes in Tri- and Perc-induced cytotoxicity than in kidney cells, with non-selective P450 inhibitors increasing toxicity. Induction of CYP2E1 with pyridine also markedly increased sensitivity of hepatocytes to Tri but had little effect on Perc-induced cytotoxicity. Increases in cellular GSH concentrations increased Tri- and Perc-induced cytotoxicity in kidney cells but not in hepatocytes, consistent with the role of GSH conjugation in Tri- and Perc-induced nephrotoxicity. in contrast, depletion of cellular GSH concentrations moderately decreased Tri- and Perc-induced cytotoxicity in kidney cells but increased cytotoxicity in hepatocytes, again pointing to the importance of different bioactivation pathways and modes of action in kidney and liver. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

  DOI：

  10.1016/j.tox.2007.03.001