L-2,6-dimethyl-oct-2ξ-enedial disemicarbazone | 93430-06-9

• 分子结构分类: 有机化合物 - 有机氮化合物
• 英文名称: L-2,6-dimethyl-oct-2ξ-enedial disemicarbazone
• 英文别名: L-2,6-Dimethyl-oct-2ξ-endial-disemicarbazon
• CAS: 93430-06-9
• 化学式: C₁₂H₂₂N₆O₂
• 分子量: 282.346
• InChiKey: NULKNAFVEBQKFP-VIFPVBQESA-N

反应信息

• 作为产物：
  描述：

  (R)-2,6-dimethyl-oct-2ξ-enedial 生成 L-2,6-dimethyl-oct-2ξ-enedial disemicarbazone
  参考文献：
  名称：

  d-和l-异丁香菊酯及其相关化合物的合成

  摘要：

  从天然的d-香茅醛开始凝视，合成了d-铱和d-异艾罗霉素。1后者在氧化作用下提供了荆芥酸，其为荆芥内酯降解产物的对映体。两个样品的混合物提供了更高熔点的外消旋物。

  DOI：

  10.1016/0040-4020(59)80003-x

文献信息

• Sites of Conditional Essential Fatty Acid Deficiency in End Stage Liver Disease
  作者：Peter A. Burke、Pei Ra. Ling、Robert A. Forse、David W. Lewis、Roger Jenkins、Bruce R. Bistrian

  DOI：10.1177/0148607101025004188

  日期：2001.7

  Background: End stage liver disease (ESLD) is a devastating illness. Its protean manifestations involve many different aspects of disturbed hepatic function. One consequence of ESLD is a decrease in plasma levels of very long chain polyunsaturated fatty acids (VL‐PUFAs), particularly arachidonic acid (AA) and docosahexaenoic acid (DHA), the former important for eicosanoid metabolism and the latter for retinal and brain membrane structure. The purpose of this study was to define the VL‐PUFA changes in liver disease by comparing plasma and tissue levels of VL‐PUFAs in controls to patients with ESLD. Methods: Fatty acid profiles from plasma, red blood cell (RBC) membranes, muscle, liver, and fat tissue from ESLD patients undergoing liver transplants were measured and compared with control patients undergoing elective liver resection. Results: Fatty acid profiles from plasma and RBC membranes showed significant decreases in AA and DHA levels in patients with ESLD compared with controls. However, there were no significant differences in tissue fatty acid composition between ESLD patients and controls. Conclusions: ESLD affects the liver's ability to maintain circulating levels of AA and DHA, and thereby presumably RBC membrane levels. However, solid tissues appear not to be affected by ESLD. Although the mechanism for these changes remains to be defined, it is consistent with hepatic impairment of elongation and desaturation to produce VL‐PUFA for transport. The present results also suggest that dietary interventions to include preformed VL‐PUFA rather than their precursors, linoleic and alpha linolenic acid, would be needed to normalize plasma VL‐PUFA levels in patients with ESLD. (journal of Parenteral and Enteral Nutrition 25:188–193, 2001)