Summerfield J A, Gollan J L, Billing B H
Biochem J. 1976 May 15;156(2):339-45. doi: 10.1042/bj1560339.
Perfusion of an isolated rat kidney with labelled bile acids, in a protein-free medium, resulted in the urinary excretion of the labelled bile acid, 3% being converted into polar metabolities in 1h. These metabolities were neither glycine nor taurine conjugates, nor bile acid glucuronides, and on solovolysis yielded the free bile acid. On t.l.c. the metabolite of [24-14C]lithocholic acid had the mobility of lithocholate 3-sulphate. The principal metabolite of [24-14C]chenodeoxycholic acid had the mobility of chenodeoxycholate 7-sulphate; trace amounts appeared as chenodeoxycholate 3-sulphate. [35S]sulphate was incorporated in chenodeoxycholic acid by the kidney, resulting in a similar pattern of sulphation. No disulphate salt of chenodeoxycholic acid was detected. These findings lend support to the hypothesis that renal synthesis may account for some of the bile acid sulphates present in urine in the cholestatic syndrome in man.
在无蛋白培养基中用标记的胆汁酸灌注离体大鼠肾脏,导致标记胆汁酸经尿液排泄,1小时内3%转化为极性代谢物。这些代谢物既不是甘氨酸也不是牛磺酸共轭物,也不是胆汁酸葡萄糖醛酸苷,经溶剂分解后产生游离胆汁酸。在薄层层析中,[24-¹⁴C]石胆酸的代谢物具有石胆酸3-硫酸盐的迁移率。[24-¹⁴C]鹅去氧胆酸的主要代谢物具有鹅去氧胆酸7-硫酸盐的迁移率;痕量以鹅去氧胆酸3-硫酸盐形式出现。肾脏将[³⁵S]硫酸盐掺入鹅去氧胆酸中,导致类似的硫酸化模式。未检测到鹅去氧胆酸的二硫酸盐。这些发现支持了以下假设:肾脏合成可能是人类胆汁淤积综合征尿液中存在的一些胆汁酸硫酸盐的原因。