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Influence of nicotinamide on the concentration of diphosphopyridine nucleotide, glycolysis and viability of ascites tumor cells following treatment with carcinostatic ethyleneimine compounds

Influence of nicotinamide on the concentration of diphosphopyridine nucleotide, glycolysis and viability of ascites tumor cells following treatment with carcinostatic ethyleneimine compounds

Biochim Et Biophys Acta 62(3): 519-524

Carcinostatic ethyleneimine compounds lower the steady state concentration of DPN in ascites tumor cells by inhibiting the biosynthesis of DPN. This is the cause for the inhibition of glycolysis. This effect is prevented by adding high concentrations of nicotinamide. Transplantation experiments have shown, however, that nicotinamide does not prevent the killing effect of carcinostatic ethyleneimine compounds on ascites tumor cells. This is explained by the fact that the physiological biosynthesis of DPN is inhibited even in presence of nicotinamide. High concentrations of nicotinamide, on the other hand, stimulate an unphysiological synthesis of DPN which compensates for the decrease of the DPN concentration caused by ethyleneimine compounds. This unphysiological synthesis of DPN ceases after washing off the nicotinamide or diluting it by transplanting the cells. Under these conditions the concentration of DPN decreases and the cells lose their viability.

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Related references

Influence of nicotinamide on the DPN-content, glycolysis and viability of ascites tumor cells after treatment with carcinostatic ethyleneimine compounds. Biochimica et Biophysica Acta 62: 519-524, 1962

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