dichloro-chlorosulfonyloxy-methyl-silane | 18170-86-0

• 分子结构分类: 有机化合物 - 有机金属化合物 - 有机类金属化合物
• 英文名称: dichloro-chlorosulfonyloxy-methyl-silane
• 英文别名: Dichlor-chlorsulfonyloxy-methyl-silan；Chloroschwefelsaeure-；[Dichloro(chlorosulfonyloxy)silyl]methane
• CAS: 18170-86-0
• 化学式: CH₃Cl₃O₃SSi
• 分子量: 229.544
• InChiKey: KZLRNTWSNGDBNT-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.53
• 重原子数：
  9
• 可旋转键数：
  2
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  51.8
• 氢给体数：
  0
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  甲基三氯硅烷 在 氯磺酸 、 三氧化硫 作用下， 生成 dichloro-chlorosulfonyloxy-methyl-silane
  参考文献：
  名称：

  Failure of BCL-2 Up-Regulation in Proximal Tubular Epithelial Cells of Donor Kidney Biopsy Specimens Is Associated with Apoptosis and Delayed Graft Function

  摘要：

  In renal transplantation, postischemic acute renal failure (ARF) develops in more than 20% of patients. We investigated whether tubular epithelial cells obtained from donor kidneys without subsequent ARF express a different pattern of survival genes, compared with cells from kidneys exhibiting ARE Donor kidney biopsy specimens were obtained before transplantation from eight recipients of cadaveric kidneys with primary graft function (CAD-PF), eight patients with biopsy-proven ARF without rejection (CAD-ARF), and eight recipients of living donor kidneys with primary graft function (LIV). One thousand proximal tubular epithelial cells per biopsy specimen were isolated by laser capture microdissection. Quantitative analysis of apoptosis and the apoptosis regulatory genes Bcl-2, Bcl-xL, and Bax were performed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-digoxigenin nick-end labeling staining and real-time PCR, respectively. Primary cultures of human proximal tubular epithelial cells served as calibrator. The number of apoptotic cells was significantly higher in CAD-ARF compared with LIV and CAD-PF (1.5 +/- 1.1% [p < 0.05] vs. 0.3 +/- 0.2% vs. 0.4 +/- 0.2%; mean +/- SD). The apoptosis inhibitors Bcl-2 and Bcl-xL were significantly up-regulated in renal tubular cells of recipients without ARF compared with CAD-ARF. The ratios of Bcl-2/GAPDH normalized to calibrator were as follows: LIV 48 +/- 30, CAD-PF 38 +/- 55, and CAD-ARF 5 +/- 7 (p < 0.05). The corresponding ratios for Bcl-xL were as follows: LIV 6 +/- 6, CAD-PF 5 +/- 3, and CAD-ARF 1 +/- 1 (p < 0.05). No difference in the expression of the proapoptotic Bax could be observed. These data suggest that failure of proximal tubular cells to respond to injury by up-regulation of survival factors from the Bcl-2 family contributes to postischemic ARF in patients after cadaveric renal transplantation.

  DOI：

  10.1097/01.lab.0000021174.66841.4c

文献信息

• Gmelin Handbuch der Anorganischen Chemie, Gmelin Handbook: S: SVol.3, 3.1.7.8.2, page 320 - 322
  作者：

  DOI：——

  日期：——
• Schmidt, M.; Schmidbaur, H., Chemische Berichte, 1962, vol. 95, p. 47 - 53
  作者：Schmidt, M.、Schmidbaur, H.

  DOI：——

  日期：——
• Failure of BCL-2 Up-Regulation in Proximal Tubular Epithelial Cells of Donor Kidney Biopsy Specimens Is Associated with Apoptosis and Delayed Graft Function
  作者：Christoph Schwarz、Peter Hauser、Rudolf Steininger、Heinz Regele、Georg Heinze、Gert Mayer、Rainer Oberbauer

  DOI：10.1097/01.lab.0000021174.66841.4c

  日期：2002.7

  In renal transplantation, postischemic acute renal failure (ARF) develops in more than 20% of patients. We investigated whether tubular epithelial cells obtained from donor kidneys without subsequent ARF express a different pattern of survival genes, compared with cells from kidneys exhibiting ARE Donor kidney biopsy specimens were obtained before transplantation from eight recipients of cadaveric kidneys with primary graft function (CAD-PF), eight patients with biopsy-proven ARF without rejection (CAD-ARF), and eight recipients of living donor kidneys with primary graft function (LIV). One thousand proximal tubular epithelial cells per biopsy specimen were isolated by laser capture microdissection. Quantitative analysis of apoptosis and the apoptosis regulatory genes Bcl-2, Bcl-xL, and Bax were performed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-digoxigenin nick-end labeling staining and real-time PCR, respectively. Primary cultures of human proximal tubular epithelial cells served as calibrator. The number of apoptotic cells was significantly higher in CAD-ARF compared with LIV and CAD-PF (1.5 +/- 1.1% [p < 0.05] vs. 0.3 +/- 0.2% vs. 0.4 +/- 0.2%; mean +/- SD). The apoptosis inhibitors Bcl-2 and Bcl-xL were significantly up-regulated in renal tubular cells of recipients without ARF compared with CAD-ARF. The ratios of Bcl-2/GAPDH normalized to calibrator were as follows: LIV 48 +/- 30, CAD-PF 38 +/- 55, and CAD-ARF 5 +/- 7 (p < 0.05). The corresponding ratios for Bcl-xL were as follows: LIV 6 +/- 6, CAD-PF 5 +/- 3, and CAD-ARF 1 +/- 1 (p < 0.05). No difference in the expression of the proapoptotic Bax could be observed. These data suggest that failure of proximal tubular cells to respond to injury by up-regulation of survival factors from the Bcl-2 family contributes to postischemic ARF in patients after cadaveric renal transplantation.