Ishikawa M, Ozaki M, Takayanagi Y, Sasaki K
Department of Pharmacology and Toxicology, Cancer Research Institute, Tohoku College of Pharmacy, Komatsushima Aobaku, Sendai, Japan.
Res Commun Chem Pathol Pharmacol. 1991 Apr;72(1):109-12.
The ability of doxapram (20 mg/kg, i.p. daily for 5 days) to induce hepatic cytochrome P-450 and xenobiotic metabolism was examined in male mice. Compared with the control values, the doxapram treatment significantly increased the amount of cytochrome P-450, and activities of aminopyrine N-demethylase, ethylmorphine N-demethylase and meperidine N-demethylase. In contrast, there were no changes in the activities of aniline hydroxylase, 7-ethoxycoumarine deethylase, NADPH-cytochrome c reductase and NADH-ferricyanide reductase, and cytochrome b5 content. These data show that there is a substrate specificity in the ability of doxapram to induce the hepatic drug metabolism in male mice.
在雄性小鼠中研究了多沙普仑（20毫克/千克，腹腔注射，每日一次，共5天）诱导肝细胞色素P - 450和外源性物质代谢的能力。与对照值相比，多沙普仑处理显著增加了细胞色素P - 450的量，以及氨基比林N - 脱甲基酶、乙基吗啡N - 脱甲基酶和哌替啶N - 脱甲基酶的活性。相比之下，苯胺羟化酶、7 - 乙氧基香豆素脱乙基酶、NADPH - 细胞色素c还原酶和NADH - 铁氰化物还原酶的活性以及细胞色素b5含量没有变化。这些数据表明，多沙普仑诱导雄性小鼠肝脏药物代谢的能力存在底物特异性。
