人胎儿肝脏中雄激素和雌激素的15-和16-羟基化：雌三醇生物合成的关键步骤。
15- and 16-hydroxylations of androgens and estrogens in the human fetal liver: a critical step in estetrol biosynthesis.
作者信息
Cantineau R, Kremers P, De Graeve J, Gielen J E, Lambotte R
出版信息
J Steroid Biochem. 1985 Feb;22(2):195-201. doi: 10.1016/0022-4731(85)90112-8.
To elucidate the main metabolic pathways which lead to the foeto-placental biosynthesis of estetrol (I), we investigated the 15 alpha- and 16 alpha-hydroxylations of potential precursors of this estrogen in the human fetal liver. We determined the 15 alpha- and 16 alpha-hydroxylation capacity of the fetal liver for each precursor by GC-MS. The results suggest that estetrol is derived only from estradiol sulfate (II) and DHEA sulfate (III). 15 alpha-Hydroxy-androstenedione (IV) can no longer be regarded as a good precursor of estetrol. The phenolic pathway appears to be a more likely route than the neutral pathway, even when derived from DHEA sulfate.
为阐明导致雌三醇（I）在胎儿 - 胎盘生物合成的主要代谢途径，我们研究了该雌激素潜在前体在人胎儿肝脏中的15α - 和16α - 羟基化作用。我们通过气相色谱 - 质谱法测定了胎儿肝脏对每种前体的15α - 和16α - 羟基化能力。结果表明，雌三醇仅来源于硫酸雌二醇（II）和硫酸脱氢表雄酮（III）。15α - 羟基雄烯二酮（IV）不再被视为雌三醇的良好前体。即使来源于硫酸脱氢表雄酮，酚类途径似乎比中性途径更可能是其合成途径。
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