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11-脱氧皮质酮诱导因子对肝癌组织培养细胞中花生四烯酸生物合成的抑制作用。

Inhibition of arachidonate biosynthesis in hepatoma tissue culture cells by 11-deoxycorticosterone-induced factor.

作者信息

Marra C A, de Alaniz M J

机构信息

Instituto de Investigaciones Bioquímicas de La Plata (INIBIOLP), CONICET-UNLP, Facultad de Ciencias Médicas, Argentina.

出版信息

Mol Cell Biochem. 1991 Apr 24;103(1):63-71. doi: 10.1007/BF00229594.

Abstract

In this work it was demonstrated that the incubation of hepatoma cultured cells (HTC 7288 c) with 11-deoxycorticosterone (DOC) ranging from 0 to 10(-4) M concentration provoked a dose-dependent inhibition in the conversion of [1-14C] eicosatrienoic acid to arachidonic acid. This steroid also produced an increase in the uptake of exogenous 20:3 (n-6) acid. The depressive effect evoked by DOC on delta 5 desaturating activity was reflected on the fatty acid composition changes of the hepatoma cells. The delta 5 desaturase activity was inhibited by a soluble factor that would be induced by the hormone and that was present in the cytosol fraction from DOC-treated cells, corresponding to a low molecular mass below 25 kDa. Presently we report that an 11-beta-OH group on the steroid molecule is not an essential requirement for the production of a delta 5 desaturase inhibitory factor.

摘要

在这项研究中,已证明将培养的肝癌细胞(HTC 7288 c)与浓度范围为0至10⁻⁴ M的11-脱氧皮质酮(DOC)一起孵育,会对[1-¹⁴C]二十碳三烯酸向花生四烯酸的转化产生剂量依赖性抑制。这种类固醇还使外源性20:3(n-6)酸的摄取增加。DOC对δ⁵去饱和活性产生的抑制作用反映在肝癌细胞的脂肪酸组成变化上。δ⁵去饱和酶活性受到一种可溶性因子的抑制,该因子由激素诱导产生,存在于经DOC处理的细胞的胞质溶胶部分中,其分子量低于25 kDa。目前我们报告,类固醇分子上的11-β-羟基并非产生δ⁵去饱和酶抑制因子的必要条件。

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