Hostetler K Y, Zenner B D, Morris H P
J Lipid Res. 1979 Jul;20(5):607-13.
Mitochondria from the 7777 hepatoma incorporate substantial amounts of l-[U-(14)C]serine into phospholipid by a Ca(2+)-dependent base-exchange reaction. This reaction is virtually absent in normal liver mitochondria. The finding cannot be attributed to microsomal contamination of the sucrose gradient-purified 7777 hepatoma mitochondria. The reaction is also absent in the rapid-growth controls, fetal rat liver and regenerating rat liver. [(14)C]Serine incorporation into 7777 hepatoma mitochondrial phospholipid by base-exchange requires Ca(2+) and is inhibited by EDTA. Ca(2+) cannot be replaced by Mg(2+), Mn(2+), or Co(2+). The reaction is inhibited by a sulfhydryl reagent and by detergents and is abolished by heating to 70 degrees C for 10 min. Product analysis indicates that phosphatidylserine and its decarboxylation product, phosphatidylethanolamine, are formed by 7777 hepatoma mitochondria, while phosphatidylserine is the sole product with microsomes. The conversion of phosphatidylserine into phosphatidylethanolamine in 7777 hepatoma mitochondria is inhibited by KCN. This study provides further evidence of abnormal mitochondrial biogenesis in the 7777 hepatoma. Our earlier study indicated a greatly increased mitochondrial activity of CTP:phosphatidate cytidylyltransferase in the 7777 hepatoma (Hostetler, Zenner, and Morris. 1978. J. Lipid Res. 19: 553-560). The presence in mitochondria of these two enzymes, which are primarily microsomal in normal liver, does not appear to be due to rapid growth alone, since their intracellular distribution was not altered in fetal or regenerating rat liver.-Hostetler, K. Y., B. D. Zenner, and H. P. Morris. Phosphatidylserine biosynthesis in mitochondria from the Morris 7777 hepatoma.
7777肝癌细胞的线粒体通过一种钙依赖的碱基交换反应将大量的L-[U-(14)C]丝氨酸掺入磷脂中。这种反应在正常肝线粒体中几乎不存在。这一发现不能归因于蔗糖梯度纯化的7777肝癌线粒体的微粒体污染。在快速生长的对照物、胎鼠肝脏和再生鼠肝脏中也不存在这种反应。通过碱基交换将[(14)C]丝氨酸掺入7777肝癌线粒体磷脂中需要钙离子，并受到乙二胺四乙酸（EDTA）的抑制。钙离子不能被镁离子、锰离子或钴离子取代。该反应受到巯基试剂和去污剂的抑制，并在加热至70摄氏度10分钟后被消除。产物分析表明，7777肝癌线粒体形成了磷脂酰丝氨酸及其脱羧产物磷脂酰乙醇胺，而微粒体的唯一产物是磷脂酰丝氨酸。7777肝癌线粒体中磷脂酰丝氨酸向磷脂酰乙醇胺的转化受到氰化钾（KCN）的抑制。这项研究为7777肝癌中线粒体生物发生异常提供了进一步的证据。我们早期的研究表明，7777肝癌中线粒体CTP：磷脂酸胞苷转移酶的活性大大增加（霍斯特特勒、泽纳和莫里斯。1978年。《脂质研究杂志》19：553 - 560）。这两种酶主要存在于正常肝脏的微粒体中，而在线粒体中的存在似乎并非仅由快速生长导致，因为它们在胎鼠或再生鼠肝脏中的细胞内分布并未改变。 - 霍斯特特勒，K.Y.，B.D.泽纳，和H.P.莫里斯。莫里斯7777肝癌线粒体中的磷脂酰丝氨酸生物合成。
