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肉瘤180细胞中磷脂酰-dCMP的代谢。氯丙嗪、磷脂酸和肌醇的作用。

Metabolism of phosphatidyl-dCMP in sarcoma 180 cells. Effect of chlorpromazine, phosphatidic acid and inositol.

作者信息

Iujvidin S, Mordoh J

出版信息

Eur J Biochem. 1986 Jan 2;154(1):187-92. doi: 10.1111/j.1432-1033.1986.tb09377.x.

Abstract

The synthesis and degradation of phosphatidyl-dCMP was studied in intact and permeabilized Sarcoma 180 cells as well as in isolated nuclei. It was verified that chlorpromazine greatly enhanced phosphatidyl-dCMP synthesis and completely abolished its hydrolysis in intact cells. The former effect was reversible and was partially lost upon permeabilization or isolation of nuclei. Phosphatidic acid also increased liponucleotide synthesis and the combination of phosphatidic acid with chlorpromazine was not additive. When inositol was added to cells which had accumulated phosphatidyl-[3H]dCMP, the recovery of radioactivity in the organic phase decreased; this effect was dose-dependent and specific for inositol, and was accompanied by an increased release of [3H]dCMP to the cell medium. In isolated microsomes, addition of Ptd-dCMP determined incorporation of [3H]inositol into phosphatidyl-inositol. These results strongly suggest that phosphatidyl-dCMP is utilized for the synthesis of phosphatidyl-inositol.

摘要

在完整的和经通透处理的肉瘤180细胞以及分离的细胞核中研究了磷脂酰 - dCMP的合成与降解。已证实氯丙嗪可极大地增强磷脂酰 - dCMP的合成,并完全消除其在完整细胞中的水解。前一种作用是可逆的,在细胞核通透或分离后会部分丧失。磷脂酸也增加了脂核苷酸的合成,且磷脂酸与氯丙嗪的联合作用并无叠加效应。当向积累了磷脂酰 - [³H]dCMP的细胞中添加肌醇时,有机相中的放射性回收率降低;这种效应呈剂量依赖性且对肌醇具有特异性,并伴有[³H]dCMP向细胞培养基中释放增加。在分离的微粒体中,添加磷脂酰 - dCMP可促使[³H]肌醇掺入磷脂酰 - 肌醇。这些结果有力地表明磷脂酰 - dCMP被用于磷脂酰 - 肌醇的合成。

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