二(三氯锌酸)4,4'-亚氨基二苯重氮化 | 9001-58-5

• 分子结构分类: 氧化还原酶 - 作用于CH-OH供体组 - 以NAD+或NADP+为受体
• 中文名称: 二(三氯锌酸)4,4'-亚氨基二苯重氮化
• 英文名称: isocitrate dehydrogenase (NAD+)
• 英文别名: isocitric dehydrogenase；beta-ketoglutaric-isocitric carboxylase；isocitric acid dehydrogenase；NAD dependent isocitrate dehydrogenase；NAD isocitrate dehydrogenase；NAD-linked isocitrate dehydrogenase；NAD-specific isocitrate dehydrogenase；NAD isocitric dehydrogenase；isocitrate dehydrogenase (NAD)；IDH (ambiguous)；nicotinamide adenine dinucleotide isocitrate dehydrogenase
• CAS: 9001-58-5

反应信息

• 作为试剂：
  描述：

  咪达唑仑 在 intestinal microsoms from Wistar rat 、 二(三氯锌酸)4,4'-亚氨基二苯重氮化 、 烟酰胺腺嘌呤双核苷酸磷酸盐 、 还原型辅酶II(NADPH)四钠盐 作用下， 以 phosphate buffer 为溶剂， 反应 0.27h， 生成 4-羟基咪达唑仑 、 1-羟基咪达唑仑
  参考文献：
  名称：

  Differential induction of midazolam metabolism in the small intestine and liver by oral and intravenous dexamethasone pretreatment in rat

  摘要：

  1. Midazolam is metabolized in the rat by CYP3A enzymes to 4-OH-midazolam (4-OH-MDZ) and 1'-OH-midazolam (1'-OH-MDZ). The induction of midazolam metabolism was studied in male Wistar rats treated with dexamethasone (50 mg kg(-1) day(-1)) during 4 days via the oral or intravenous routes. Microsomes were prepared from the liver and the proximal small intestine and in vitro metabolism of midazolam was determined. In addition, CYP3A1- and CYP3A2-like protein levels were measured by gel electrophoresis and immunoblotting.2. The V-max's (mean SEM) for 4-OH-MDZ and 1'-OH-MDZ formation were much lower in intestinal (0.078 +/- 0.002 and 0.074 +/- 0.002 muM min(-1) mg(-1) protein, respectively) compared with hepatic microsomes prepared from the uninduced rat (0.870 +/- 0.007 and 0.310 +/- 0.020 muM min(-1) mg-1 protein, respectively). Induction by oral or intravenous dexamethasone pretreatment led to significant increases in V-max for 4-OH-MDZ and VOH-MDZ by both intestinal and hepatic microsomes. Oral dexamethasone pretreatment via the oral route resulted in a more pronounced increase in compared with intravenous administration of the inducer.3. CYP3A1 and CYP3A2 protein levels in liver microsomes were significantly increased following oral (3.7- and 3.2-fold, respectively) or intravenous (2.6- and 2.1-fold, respectively) pretreatment with dexamethasone. On the contrary, only oral dexamethasone pretreatment resulted in a significant change in intestinal CYP3A2-hke protein (7.3-fold). A slight difference in the migration distance of the immunoreactive band for CYP3A2 was also observed for intestinal microsomes.4. These results suggest that intestinal CYP3A enzymes in the rat differ from hepatic CYP3A1 and CYP3A2. They also demonstrate that systemic dexamethasone administration can induce intestinal microsome activity.

  DOI：

  10.1080/0049825021000012655