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9
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本文引用的文献

1
A family and population study of the genetic polymorphism of debrisoquine oxidation in a white British population.对英国白人人群中异喹胍氧化遗传多态性的家系及群体研究。
J Med Genet. 1980 Apr;17(2):102-5. doi: 10.1136/jmg.17.2.102.
2
Purification and characterization of the rat liver microsomal cytochrome P-450 involved in the 4-hydroxylation of debrisoquine, a prototype for genetic variation in oxidative drug metabolism.参与异喹胍4-羟化反应的大鼠肝脏微粒体细胞色素P-450的纯化与特性研究,异喹胍是氧化药物代谢遗传变异的一个原型。
Biochemistry. 1984 Jun 5;23(12):2787-95. doi: 10.1021/bi00307a039.
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Inherited defects of hepatic drug metabolism.
Semin Liver Dis. 1983 Nov;3(4):341-54. doi: 10.1055/s-2008-1040786.
4
Dextromethorphan as a safe probe for debrisoquine hydroxylation polymorphism.右美沙芬作为去甲丙咪嗪羟化多态性的安全探针。
Lancet. 1984 Sep 1;2(8401):517-8. doi: 10.1016/s0140-6736(84)92591-1.
5
Polymorphic dextromethorphan metabolism: co-segregation of oxidative O-demethylation with debrisoquin hydroxylation.多态性右美沙芬代谢:氧化O-去甲基化与异喹胍羟基化的共分离。
Clin Pharmacol Ther. 1985 Dec;38(6):618-24. doi: 10.1038/clpt.1985.235.
6
Purification and characterization of the human liver cytochromes P-450 involved in debrisoquine 4-hydroxylation and phenacetin O-deethylation, two prototypes for genetic polymorphism in oxidative drug metabolism.参与异喹胍4-羟化和非那西丁O-脱乙基反应的人肝细胞色素P-450的纯化与特性分析,这两个反应是氧化药物代谢中遗传多态性的两个原型。
J Biol Chem. 1985 Jul 25;260(15):9057-67.
7
Polymorphic hydroxylation of Debrisoquine in man.人对异喹胍的多态性羟基化作用。
Lancet. 1977 Sep 17;2(8038):584-6. doi: 10.1016/s0140-6736(77)91430-1.

法国人群中右美沙芬氧化的多态性。

Polymorphism of dextromethorphan oxidation in a French population.

作者信息

Larrey D, Amouyal G, Tinel M, Letteron P, Berson A, Labbe G, Pessayre D

机构信息

Unité de Recherches de Physiopathologie Hépatique (INSERM U 24), Hôpital Beaujon, Clichy, France.

出版信息

Br J Clin Pharmacol. 1987 Nov;24(5):676-9. doi: 10.1111/j.1365-2125.1987.tb03230.x.

DOI:10.1111/j.1365-2125.1987.tb03230.x
PMID:3435696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1386343/
Abstract

Genetically-controlled drug oxidation capacity was studied using dextromethorphan, an anti-tussive drug, as the test compound in 103 healthy white French subjects (61 males and 42 females). Phenotyping was performed using the metabolic ratio (MR) calculated as MR = 0-10 h urinary output of dextromethorphan/0-10 h urinary output of dextrorphan, after oral administration of 40 mg (113.6 mumol) of dextromethorphan hydrobromide. The log MR was bimodally distributed: 99 subjects (96.1%) were phenotyped as extensive metabolizers; they had a log MR between -3.1 and -1.1, a urinary output of dextromethorphan below 5 mumol 10 h-1 and a urinary output of dextrorphan above 20 mumol 10 h-1. Four subjects (3.9%) were phenotyped as poor metabolizers; they had a log MR between -0.5 and +0.7, a urinary output of dextromethorphan above 5 mumol 10 h-1 and a urinary out of dextrorphan below 20 mumol 10 h-1.

摘要

以止咳药右美沙芬作为测试化合物,对103名健康的法国白人受试者(61名男性和42名女性)的基因控制药物氧化能力进行了研究。口服40毫克(113.6微摩尔)氢溴酸右美沙芬后,使用代谢比(MR)进行表型分析,代谢比的计算方法为MR = 右美沙芬0至10小时尿量/右啡烷0至10小时尿量。对数MR呈双峰分布:99名受试者(96.1%)被表型为快代谢者;他们的对数MR在-3.1至-1.1之间,右美沙芬尿量低于5微摩尔/10小时,右啡烷尿量高于20微摩尔/10小时。4名受试者(3.9%)被表型为慢代谢者;他们的对数MR在-0.5至+0.7之间,右美沙芬尿量高于5微摩尔/10小时,右啡烷尿量低于20微摩尔/10小时。