In DBAH1 tumor, DBAG tumor, and Novikoff hepatoma, both aerobic and anaerobic glycolysis were stimulated by increasing the glucose concentration from 0.5 to 5 mm. Therefore, it was concluded that the availability of intracellular glucose was a rate-limiting factor for glycolysis. In these 3 tumors, the difference between the rates of aerobic and anaerobic lactate production was primarily due to a more severe inhibition of P-fructokinase3 activity under aerobic conditions. Thus, P-fructokinase was at least partially responsible for the Pasteur effect. In addition, the inhibition of P-fructokinase resulted in an accumulation of glucose-6-P, which then inhibited hexokinase activity.

In Novikoff ascites tumor cells, after the addition of glucose, rate-limiting factors for glycolysis and the levels of intracellular intermediates were found to change continuously with the time of incubation. Factors responsible for the Pasteur effect also change with the length of incubation. Under anaerobic conditions, striking parallism between the rate of lactate production and the level of intracellular Pi concentration were observed at every time interval.

In all 4 types of tumors, Pi transport can be facilitated by both the glycolytic and the respiratory energy. This appears to be a unique feature of all tumors studied so far, since normal cells examined to date can use only respiratory energy for Pi transport.


This investigation was supported by Public Health Service Research Grant CA-05706 from the National Cancer Institute, and by Grant DA-AMC-18-035-70(A) from the U.S. Army Chemical Center Procurement Agency.


The following abbreviations are used: P (in combinations), phosphate (phospho-); Pi, inorganic phosphate; AMP and ATP, the mono- and triphosphates of adenosine.

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