尿胆汁酸和胆汁醇排泄不能反映异喹胍羟基化的遗传多态性。
Urinary bile acid and bile alcohol excretion does not reflect the genetic polymorphism of debrisoquine hydroxylation.
作者信息
Karlaganis G, Küpfer A, Preisig R
出版信息
Br J Clin Pharmacol. 1984 Apr;17(4):470-3. doi: 10.1111/j.1365-2125.1984.tb02374.x.
Abstract
Excretion of the major urinary bile alcohol 27-nor-5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 24,25- pentol , and of cholic, chenodeoxycholic, deoxycholic and lithocholic acid was measured in 24 h urine collections of 10 extensive and seven poor metabolizers of debrisoquine. There was no significant difference of the excretion of these cholesterol metabolites between the two groups, indicating that cholesterol hydroxylation to bile alcohols and bile acids is probably not controlled by the same genes responsible for the 'debrisoquine-type' hydroxylation polymorphism.
摘要
在对10名异喹胍广泛代谢者和7名异喹胍弱代谢者进行的24小时尿液收集检测中，测定了主要尿胆汁醇27-去甲-5β-胆甾烷-3α,7α,12α,24,25-戊醇以及胆酸、鹅去氧胆酸、脱氧胆酸和石胆酸的排泄情况。两组之间这些胆固醇代谢产物的排泄没有显著差异，这表明胆固醇羟基化生成胆汁醇和胆汁酸的过程可能不受负责“异喹胍型”羟基化多态性的相同基因控制。
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Pharmacogenetic covariation of defective N-oxidation of sparteine and 4-hydroxylation of debrisoquine.司巴丁N-氧化缺陷与异喹胍4-羟化的药物遗传学共变。
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Hydroxylations in biosynthesis and metabolism of bile acids. Catalytic properties of different forms of cytochrome P-450.胆汁酸生物合成与代谢中的羟化作用。不同形式细胞色素P-450的催化特性。
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