Hostetler K Y, Zenner B D, Morris H P
J Lipid Res. 1978 Jul;19(5):553-60.
The subcellular and submitochondrial localization of CTP:phosphatidate cytidylyltransferase is altered in the Morris 7777 hepatoma. Mitochondria in this poorly differentiated tumor are the principal sites of CDP-diacylglycerol synthesis, in contrast to normal rat liver where the endoplasmic reticulum is most active. This enzyme activity was increased 17-fold in the outer mitochondrial membrane, and a 22% increase was noted in the inner mitochondrial membrane of the 7777 hepatoma as compared with the corresponding fractions from normal rat liver. Increased mitochondrial CTP:phosphatidate cytidylyltransferase was present in six other Morris hepatomas, but it was not found in fetal rat liver mitochondria, suggesting that rapid growth alone is not responsible for the difference. Evidence is presented which indicates that mitochondrial lipid degradation is similar in normal liver and the 7777 hepatoma, in vitro. The increased activity of CTP: phosphatidate cytidylytransferase is thought to be responsible in part for the moderately increased diphosphatidylglycerol content of 7777 hepatoma mitochondria.
磷脂酸胞苷转移酶的亚细胞及亚线粒体定位在莫里斯7777肝癌中发生了改变。与内质网最为活跃的正常大鼠肝脏相反，在这种低分化肿瘤中，线粒体是CDP - 二酰基甘油合成的主要场所。与正常大鼠肝脏的相应组分相比，该酶活性在线粒体外膜中增加了17倍，在7777肝癌的线粒体内膜中增加了22%。在其他六种莫里斯肝癌中也存在线粒体CTP：磷脂酸胞苷转移酶活性增加的情况，但在胎鼠肝脏线粒体中未发现，这表明单纯的快速生长并非造成这种差异的原因。本文提供的证据表明，在体外，正常肝脏和7777肝癌中线粒体脂质降解情况相似。CTP：磷脂酸胞苷转移酶活性的增加被认为部分导致了7777肝癌线粒体中二磷脂酰甘油含量的适度增加。
