Marra C A, de Alaniz M J, Brenner R R
Mol Cell Biochem. 1985 Jan;65(2):143-52. doi: 10.1007/BF00221097.
The incorporation and conversion of eicosa-8,11,14-trienoic acid to arachidonic acid were studied in HTC cells (7288 c hepatoma cells) and isolated hepatocytes of rat. The cells were incubated at different concentrations of the acid during 0 to 6 hours. Both kinds of cells were able to take up the acid. However, the HTC cells have a greater avidity for the eicosatrienoic acid than normal liver cells. The incorporation of the acid modified the fatty acid composition of the cells and caused a decrease in the amount of saturated and monoenoic acid. In both cells eicosatrienoic acid was converted to arachidonic acid. However, in HTC cells arachidonic acid level was low and not correlated with the amount of the eicosatrienoic acid incorporated. This fact is apparently not due to an impairment in delta 5 desaturation activity since this enzyme is active in both cells. It would be possible that arachidonic acid production in malignant cells would be also interrupted in another metabolic pathway after delta 6 desaturation step. The strikingly low amount of arachidonic acid biosynthesized in HTC cells compared to normal hepatocytes could be interpreted as a consequence of a lower availability of eicosatrienoic acid for the microsomal desaturation system in malignant cells, in addition to the low delta 6 desaturase activity.
在HTC细胞(7288c肝癌细胞)和大鼠分离的肝细胞中研究了二十碳-8,11,14-三烯酸向花生四烯酸的掺入和转化。细胞在不同浓度的该酸中孵育0至6小时。两种细胞都能够摄取该酸。然而,HTC细胞对二十碳三烯酸的亲和力比正常肝细胞更高。该酸的掺入改变了细胞的脂肪酸组成,并导致饱和脂肪酸和单不饱和脂肪酸含量降低。在两种细胞中,二十碳三烯酸都转化为花生四烯酸。然而,在HTC细胞中,花生四烯酸水平较低,且与掺入的二十碳三烯酸量无关。这一事实显然不是由于δ5去饱和活性受损,因为该酶在两种细胞中均有活性。有可能恶性细胞中花生四烯酸的产生在δ6去饱和步骤之后的另一条代谢途径中也会被中断。与正常肝细胞相比,HTC细胞中生物合成的花生四烯酸量极低,这除了δ6去饱和酶活性较低外,还可以解释为恶性细胞微粒体去饱和系统中二十碳三烯酸的可用性较低的结果。