Suppr超能文献

替拉米特的体外代谢。I. 人及大鼠肝脏微粒体对替拉米特的氧化代谢

Metabolism of tiaramide in vitro. I. Oxidative metabolism of tiaramide by human and rat liver microsomes.

作者信息

Iwasaki K, Noguchi H, Kamataki T, Kato R

出版信息

Xenobiotica. 1982 Apr;12(4):221-6. doi: 10.3109/00498258209052459.

Abstract
  1. N-Dealkylation and N-oxidation of tiaramide and of its major metabolite, TRAA, by human and rat liver microsomes were investigated. 2. With human liver microsomes, N-oxidation of tiaramide was 1.5-8.0 times faster than N-dealkylation. N-Oxidation of the metabolite, TRAA, by human liver microsomes was much slower than that of tiaramide. The high recovery of tertiary amine N-oxides in human urine after tiaramide dosing reflects the high activity of N-oxidation of tiaramide by human liver microsomes. 3. Phenobarbital treatment of rats caused an increase in the liver microsomal N-dealkylation of tiaramide in vitro, but had little effect on N-oxidation. 3-Methylcholanthrene treatment of rats caused decrease of both reactions. 4. Metyrapone added to rat liver microsomes inhibited N-dealkylation more strongly than N-oxidation. Tetrahydrofuran and 7,8-benzoflavone inhibited N-dealkylation but had little effect on N-oxidation. Addition to the microsomal incubations of antisera against NADPH-cytochrome c reductase caused marked inhibition of N-dealkylation and slight inhibition of N-oxidation.
摘要
  1. 研究了人及大鼠肝微粒体对替拉米特及其主要代谢物TRAA的N-脱烷基化和N-氧化作用。2. 对于人肝微粒体,替拉米特的N-氧化比N-脱烷基化快1.5至8.0倍。人肝微粒体对代谢物TRAA的N-氧化比替拉米特的N-氧化慢得多。替拉米特给药后,人尿中叔胺N-氧化物的高回收率反映了人肝微粒体对替拉米特N-氧化的高活性。3. 用苯巴比妥处理大鼠导致体外肝微粒体对替拉米特的N-脱烷基化增加,但对N-氧化作用影响很小。用3-甲基胆蒽处理大鼠导致两种反应均降低。4. 添加到大鼠肝微粒体中的美替拉酮对N-脱烷基化的抑制作用比对N-氧化的抑制作用更强。四氢呋喃和7,8-苯并黄酮抑制N-脱烷基化,但对N-氧化作用影响很小。向微粒体孵育体系中添加抗NADPH-细胞色素c还原酶的抗血清会导致N-脱烷基化受到显著抑制,N-氧化受到轻微抑制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验