3-异丙基-2,6,6-三甲基-庚-4-炔-3-醇 | 100544-90-9

• 分子结构分类: 有机化合物 - 有机氧化合物
• 中文名称: 3-异丙基-2,6,6-三甲基-庚-4-炔-3-醇
• 英文名称: 3-isopropyl-2,6,6-trimethyl-hept-4-yn-3-ol
• 英文别名: 3-Isopropyl-2,6,6-trimethyl-hept-4-in-3-ol；2,6,6-Trimethyl-3-propan-2-ylhept-4-yn-3-ol
• CAS: 100544-90-9
• 化学式: C₁₃H₂₄O
• 分子量: 196.333
• InChiKey: DGLAVMAMCUOMQR-UHFFFAOYSA-N

物化性质

• 沸点：
  75.5 °C(Press: 5 Torr)
• 密度：
  0.8334 g/cm3

计算性质

• 辛醇/水分配系数(LogP)：
  4
• 重原子数：
  14
• 可旋转键数：
  4
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.85
• 拓扑面积：
  20.2
• 氢给体数：
  1
• 氢受体数：
  1

反应信息

• 作为反应物：
  描述：

  3-异丙基-2,6,6-三甲基-庚-4-炔-3-醇 在 盐酸 作用下， 生成 3-isopropyl-2,6,6-trimethyl-hept-2-en-4-yne
  参考文献：
  名称：

  Abnormal Iron Deposition in Renal Cells in the Rat with Chronic Angiotensin II Administration

  摘要：

  Acute experimental iron loading causes iron to accumulate in the renal tissue. The accumulation of iron may play a role in enhancing oxidant-induced tubular injury by producing increased amounts of reactive oxygen species. From findings in cells from heme oxygenase-1 (HO-1) -deficient mice, HO-1 is postulated to prevent abnormal intracellular iron accumulation. Recently, it has been reported that HO-1 is induced in the renal tubular epithelial cells, in which iron is deposited after iron loading, and that this HO-1 induction may be involved in ameliorating iron-induced renal toxicity. We previously showed that chronic administration of angiotensin II to rats induces HO-1 expression in the tubular epithelial cells. These observations led us to investigate whether there is a link between iron deposition and HO-1 induction in renal tubular cells in rats undergoing angiotensin II infusion. In the present study, rats were given angiotensin II for continuously 7 days. Prussian blue staining revealed the distinct deposits of iron in the proximal tubular epithelial cells after angiotensin II administration. Electron microscopy demonstrated that iron particles were present in the lysosomes of these cells. Histologic and immunohistochemical analyses showed that stainable iron and immunoreactive ferritin and HO-1 were colocalized in the tubular epithelial cells. Treatment of angiotensin II-infused rats with an iron chelator, deferoxamine, blocked the abnormal iron deposition in kidneys and also the induced expression of HO-1 and ferritin expression. Furthermore, deferoxamine treatment suppressed the angiotensin II-induced increase in the urinary excretion of protein and N-acetyl-beta-D-glucosaminidase, a marker of tubular injury; however, deferoxamine did not affect the angiotensin II-induced decrease in glomerular filtration rate. These results suggest that angiotensin II causes renal injury, in part, by inducing the deposition of iron in the kidney.

  DOI：

  10.1038/labinvest.3780398
• 作为产物：
  描述：

  2,4-二甲基-3-戊酮 、 tert-butyllithium 生成 3-异丙基-2,6,6-三甲基-庚-4-炔-3-醇
  参考文献：
  名称：

  溴甲基二甲基甲硅烷基二异丙基丙炔醚的5-Endo-Trig自由基环化。对功能性环戊烷的高度非对映选择性。

  摘要：

  一个有效的自由基序列，涉及5-exo-dig，非对映选择性的1,5-H转移以及在全碳系统中很少观察到的5-endo-trig环化，使得环戊基衍生物2的结构可以由四个受控的立体异构中心组成二异丙基前体1.还分离了烯烃3作为次要副产物。已经研究了炔基取代基Y的作用，并描述了级联的范围和限制。

  DOI：

  10.1021/jo9904260

文献信息

• 5-<i>E</i><i>ndo</i>-<i>T</i><i>rig</i> Radical Cyclizations of Bromomethyldimethylsilyl Diisopropylpropargylic Ethers. A Highly Diastereoselective Access to Functionalized Cyclopentanes
  作者：Stéphane Bogen、Mihaela Gulea、Louis Fensterbank、Max Malacria

  DOI：10.1021/jo9904260

  日期：1999.6.1

  An efficient radical sequence involving a 5-exo-dig, a diastereoselective 1,5-H transfer, and a rarely observed in an all-carbon system 5-endo-trig cyclization allows the construction of cyclopentyl derivatives 2 bearing four controlled stereogenic centers from diisopropyl precursors 1. Olefins 3 were also isolated as minor side products. The effect of the acetylenic substituent Y has been investigated

  一个有效的自由基序列，涉及5-exo-dig，非对映选择性的1,5-H转移以及在全碳系统中很少观察到的5-endo-trig环化，使得环戊基衍生物2的结构可以由四个受控的立体异构中心组成二异丙基前体1.还分离了烯烃3作为次要副产物。已经研究了炔基取代基Y的作用，并描述了级联的范围和限制。
• Abnormal Iron Deposition in Renal Cells in the Rat with Chronic Angiotensin II Administration
  作者：Nobukazu Ishizaka、Toru Aizawa、Ieharu Yamazaki、Shin-ichi Usui、Ichiro Mori、Kiyoshi Kurokawa、Shiow-Shih Tang、Julie R Ingelfinger、Minoru Ohno、Ryozo Nagai

  DOI：10.1038/labinvest.3780398

  日期：2002.1

  Acute experimental iron loading causes iron to accumulate in the renal tissue. The accumulation of iron may play a role in enhancing oxidant-induced tubular injury by producing increased amounts of reactive oxygen species. From findings in cells from heme oxygenase-1 (HO-1) -deficient mice, HO-1 is postulated to prevent abnormal intracellular iron accumulation. Recently, it has been reported that HO-1 is induced in the renal tubular epithelial cells, in which iron is deposited after iron loading, and that this HO-1 induction may be involved in ameliorating iron-induced renal toxicity. We previously showed that chronic administration of angiotensin II to rats induces HO-1 expression in the tubular epithelial cells. These observations led us to investigate whether there is a link between iron deposition and HO-1 induction in renal tubular cells in rats undergoing angiotensin II infusion. In the present study, rats were given angiotensin II for continuously 7 days. Prussian blue staining revealed the distinct deposits of iron in the proximal tubular epithelial cells after angiotensin II administration. Electron microscopy demonstrated that iron particles were present in the lysosomes of these cells. Histologic and immunohistochemical analyses showed that stainable iron and immunoreactive ferritin and HO-1 were colocalized in the tubular epithelial cells. Treatment of angiotensin II-infused rats with an iron chelator, deferoxamine, blocked the abnormal iron deposition in kidneys and also the induced expression of HO-1 and ferritin expression. Furthermore, deferoxamine treatment suppressed the angiotensin II-induced increase in the urinary excretion of protein and N-acetyl-beta-D-glucosaminidase, a marker of tubular injury; however, deferoxamine did not affect the angiotensin II-induced decrease in glomerular filtration rate. These results suggest that angiotensin II causes renal injury, in part, by inducing the deposition of iron in the kidney.