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.