(2,2,2-trichloro-ethyl)-phosphonic acid-dichloride | 99584-50-6

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 有机膦酸及其衍生物
• 英文名称: (2,2,2-trichloro-ethyl)-phosphonic acid-dichloride
• 英文别名: (2,2,2-Trichlor-aethyl)-phosphonsaeure-dichlorid；P-(2,2,2-Trichloroethyl)phosphonic dichloride；1,1,1-trichloro-2-dichlorophosphorylethane
• CAS: 99584-50-6
• 化学式: C₂H₂Cl₅OP
• 分子量: 250.276
• InChiKey: FEVFRYLSYMOUIG-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.8
• 重原子数：
  9
• 可旋转键数：
  1
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  17.1
• 氢给体数：
  0
• 氢受体数：
  1

反应信息

• 作为反应物：
  描述：

  (2,2,2-trichloro-ethyl)-phosphonic acid-dichloride 、 苯胺 生成 (2,2,2-trichloro-ethyl)-phosphonic acid anilide chloride
  参考文献：
  名称：

  in vivo Cell Lineage Analysis During Chemical Hepatocarcinogenesis in Rats Using Retroviral-Mediated Gene Transfer: Evidence for Dedifferentiation of Mature Hepatocytes

  摘要：

  Feeding adult rats with a diet containing 2-acetylaminofluorene (2-AAF) results in suppression of hepatocyte proliferation and stimulation of oval cell proliferation. Although oval cells may be facultative liver stem cells, the actual relationship between oval cells and liver cancer has not been clearly established in vivo. Our goal was to label hepatic cells in vivo using retroviral vectors and follow their fate during the early steps of chemically induced hepatocarcinogenesis. Oval cell proliferation was induced by continuous feeding with a carcinogenic diet containing 2-AAF. We used two different strategies to genetically label hepatic cells: (a) labeling of proliferating cells in rats fed 2-AAF by injecting recombinant retroviral vectors containing the beta-galactosidase gene either in a peripheral vein or in the common bile duct at the peak of oval cell proliferation and (b) prelabeling of hepatocytes by intravenously injecting recombinant vectors 1 day after partial hepatectomy and 1 week before subsequent administration of 2-AAF. Using the first strategy, transgene expression occurred in both oval cells and hepatocytes. Using the second strategy, we could selectively label, and hence study the fate of, differentiated hepatocytes. In the latter case, we observed clusters of beta-galactosidase-positive hepatocytes, some of them also expressing preneoplastic markers such as gamma-glutamyl transpeptidase as well as the placental form of glutathione-S-transferase. These results demonstrate that preneoplastic foci can originate from mature hepatocytes and are consistent with the hypothesis that dedifferentiation of mature hepatocytes may occur during the course of carcinogenic regimen.

  DOI：

  10.1097/01.lab.0000017363.11489.ad
• 作为产物：
  描述：

  三氯乙烯 在 三氯化铝 、 三氯化磷 作用下， 生成 (2,2,2-trichloro-ethyl)-phosphonic acid-dichloride
  参考文献：
  名称：

  in vivo Cell Lineage Analysis During Chemical Hepatocarcinogenesis in Rats Using Retroviral-Mediated Gene Transfer: Evidence for Dedifferentiation of Mature Hepatocytes

  摘要：

  Feeding adult rats with a diet containing 2-acetylaminofluorene (2-AAF) results in suppression of hepatocyte proliferation and stimulation of oval cell proliferation. Although oval cells may be facultative liver stem cells, the actual relationship between oval cells and liver cancer has not been clearly established in vivo. Our goal was to label hepatic cells in vivo using retroviral vectors and follow their fate during the early steps of chemically induced hepatocarcinogenesis. Oval cell proliferation was induced by continuous feeding with a carcinogenic diet containing 2-AAF. We used two different strategies to genetically label hepatic cells: (a) labeling of proliferating cells in rats fed 2-AAF by injecting recombinant retroviral vectors containing the beta-galactosidase gene either in a peripheral vein or in the common bile duct at the peak of oval cell proliferation and (b) prelabeling of hepatocytes by intravenously injecting recombinant vectors 1 day after partial hepatectomy and 1 week before subsequent administration of 2-AAF. Using the first strategy, transgene expression occurred in both oval cells and hepatocytes. Using the second strategy, we could selectively label, and hence study the fate of, differentiated hepatocytes. In the latter case, we observed clusters of beta-galactosidase-positive hepatocytes, some of them also expressing preneoplastic markers such as gamma-glutamyl transpeptidase as well as the placental form of glutathione-S-transferase. These results demonstrate that preneoplastic foci can originate from mature hepatocytes and are consistent with the hypothesis that dedifferentiation of mature hepatocytes may occur during the course of carcinogenic regimen.

  DOI：

  10.1097/01.lab.0000017363.11489.ad

文献信息

• Sinow'ew; Soborowskii, Zhurnal Obshchei Khimii, 1959, vol. 29, p. 2643,2645;engl.Ausg.S.2607
  作者：Sinow'ew、Soborowskii

  DOI：——

  日期：——
• in vivo Cell Lineage Analysis During Chemical Hepatocarcinogenesis in Rats Using Retroviral-Mediated Gene Transfer: Evidence for Dedifferentiation of Mature Hepatocytes
  作者：Jérôme Gournay、Isabelle Auvigne、Virginie Pichard、Catherine Ligeza、Marie-Pierre Bralet、Nicolas Ferry

  DOI：10.1097/01.lab.0000017363.11489.ad

  日期：2002.6

  Feeding adult rats with a diet containing 2-acetylaminofluorene (2-AAF) results in suppression of hepatocyte proliferation and stimulation of oval cell proliferation. Although oval cells may be facultative liver stem cells, the actual relationship between oval cells and liver cancer has not been clearly established in vivo. Our goal was to label hepatic cells in vivo using retroviral vectors and follow their fate during the early steps of chemically induced hepatocarcinogenesis. Oval cell proliferation was induced by continuous feeding with a carcinogenic diet containing 2-AAF. We used two different strategies to genetically label hepatic cells: (a) labeling of proliferating cells in rats fed 2-AAF by injecting recombinant retroviral vectors containing the beta-galactosidase gene either in a peripheral vein or in the common bile duct at the peak of oval cell proliferation and (b) prelabeling of hepatocytes by intravenously injecting recombinant vectors 1 day after partial hepatectomy and 1 week before subsequent administration of 2-AAF. Using the first strategy, transgene expression occurred in both oval cells and hepatocytes. Using the second strategy, we could selectively label, and hence study the fate of, differentiated hepatocytes. In the latter case, we observed clusters of beta-galactosidase-positive hepatocytes, some of them also expressing preneoplastic markers such as gamma-glutamyl transpeptidase as well as the placental form of glutathione-S-transferase. These results demonstrate that preneoplastic foci can originate from mature hepatocytes and are consistent with the hypothesis that dedifferentiation of mature hepatocytes may occur during the course of carcinogenic regimen.