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培养的人绒毛膜癌中由C19前体生成雌激素。

Oestrogen formation from C19 precursors in human choriocarcinoma in culture.

作者信息

Schut H A, Townsley J D

出版信息

Acta Endocrinol (Copenh). 1977 Mar;84(3):633-41. doi: 10.1530/acta.0.0840633.

Abstract

A cloned cell line of human choriocarcinoma was evaluated as a model of human placental oestrogen production. Oestrone formation from dehydroepiandrosterone (D), D-sulphate (DS) or 4-androstenedione (A) was less than or equal to 5% of oestradiol-17beta (Oe2) formation. Oe2 formation from D and A was similar (100-150 pmole/h/10(7) cells); that from DS was 10 times less. Omitting serum from the medium increased Oe2 yield from DS 4-fold; addition of albumin restored these yields to control values (P greater than 0.05, t-test), presumably by binding DS. N6,O2'-dibutyryl-adenosine 3',5'-cyclic monophosphoric acid and theophylline treatment for 72 h stimulated (P less than 0.01) Oe2 formation from D (36%), DS (66%) and A (183%). In intact cells, sulphatase activity, Oe2 formation from D and Oe2 formation from DS equalled those in homogenates (P greater than 0.05) but Oe2 formation from D was greater than that from DS in both systems (P less than 0.001), indicating a deficiency of sulphatase relative to subsequent enzymes of oestrogen synthesis. Steroids, at concentrations previously shown to inhibit placental sulphatase or 3beta-hydroxysteroid dehydrogenase, did not inhibit choriocarcinoma enzymes. Except for its relative sulphatase deficiency and insusceptibility of oestrogen synthesizing enzymes to steroid inhibitors, choriocarcinoma appears to be a useful model of placental oestrogen synthesis.

摘要

对一株人绒毛膜癌克隆细胞系进行了评估,以作为人胎盘雌激素生成的模型。由脱氢表雄酮(D)、硫酸脱氢表雄酮(DS)或4-雄烯二酮(A)生成雌酮的量小于或等于雌二醇-17β(Oe2)生成量的5%。由D和A生成Oe2的量相似(100 - 150皮摩尔/小时/10⁷个细胞);由DS生成的量则少10倍。从培养基中去除血清可使由DS生成的Oe2产量增加4倍;添加白蛋白可使这些产量恢复到对照值(P>0.05,t检验),推测是通过结合DS实现的。用N6,O2'-二丁酰-腺苷3',5'-环磷酸和茶碱处理72小时可刺激(P<0.01)由D(36%)、DS(66%)和A(183%)生成Oe2。在完整细胞中,硫酸酯酶活性、由D生成Oe2的量以及由DS生成Oe2的量与匀浆中的相等(P>0.05),但在两个系统中由D生成Oe2的量均大于由DS生成的量(P<0.001),这表明相对于雌激素合成的后续酶,硫酸酯酶存在缺陷。以前显示可抑制胎盘硫酸酯酶或3β-羟基类固醇脱氢酶的类固醇浓度,并未抑制绒毛膜癌细胞系的酶。除了其相对的硫酸酯酶缺陷以及雌激素合成酶对类固醇抑制剂不敏感外,绒毛膜癌似乎是胎盘雌激素合成的一个有用模型。

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