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腹水肿瘤血浆脂蛋白对艾氏腹水癌细胞中脂肪酸生物合成的调节作用。

Regulation of fatty acid biosynthesis in Ehrlich cells by ascites tumor plasma lipoproteins.

作者信息

McGee R, Brenneman D E, Spector A A

出版信息

Lipids. 1977 Jan;12(1):66-74. doi: 10.1007/BF02532975.

Abstract

Fatty acid biosynthesis in Ehrlich cells in vitro was reduced when very low density lipoproteins (VLDL) isolated from the ascites tumor plasma were added to the incubation medium. The degree of inhibition was dependent on the VLDL concentration. At the VLDL concentrations usually present in the ascites plasma, there was a 30% decrease in biosynthesis as measured by (3)H(2)O incorporation into fatty acids. Analysis of the labeled fatty acids by gas liquid chromatography indicated that this decrease was due to a reduction in fatty acid de novo biosynthesis and that chain elongation actually was increased when VLDL were present. Although ascites plasma low- and high density lipoproteins also produced a concentration-dependent inhibition of fatty acid biosynthesis, their effects were much smaller than those of the VLDL. Studies employing VLDL and radioactive free fatty acids indicated that the cells took up utlilzed fatty acids derived from these lipoproteins. When VLDL were present, labeled free fatty acid incorporation into cell phospholipids, cholesteryl esters, and CO(2) decreased, whereas its incorporation into the cell free fatty acid pool increased. By contrast, the cells incorporated only very small amounts of fatty acid from either low- or high density lipoproteins. This suggests that the VLDL exert their inhibitory effect on fatty acid synthesis by supplying exogenous fatty acids to the cells.

摘要

当将从腹水肿瘤血浆中分离出的极低密度脂蛋白(VLDL)添加到培养介质中时,体外艾氏腹水癌细胞中的脂肪酸生物合成会减少。抑制程度取决于VLDL的浓度。在腹水血浆中通常存在的VLDL浓度下,通过将(3)H(2)O掺入脂肪酸来测量,生物合成减少了30%。通过气相色谱法对标记脂肪酸进行分析表明,这种减少是由于脂肪酸从头生物合成的减少,并且当存在VLDL时,链延长实际上增加了。尽管腹水血浆中的低密度和高密度脂蛋白也会产生浓度依赖性的脂肪酸生物合成抑制作用,但其作用比VLDL小得多。使用VLDL和放射性游离脂肪酸的研究表明,细胞摄取并利用了这些脂蛋白衍生的脂肪酸。当存在VLDL时,标记的游离脂肪酸掺入细胞磷脂、胆固醇酯和CO(2)的量减少,而其掺入细胞游离脂肪酸池的量增加。相比之下,细胞从低密度或高密度脂蛋白中仅掺入极少量的脂肪酸。这表明VLDL通过向细胞提供外源性脂肪酸来对脂肪酸合成发挥抑制作用。

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