THE ROLE OF DPN ase IN THE MECHANISM OF ACTION OF AN ANTITUMOR ALKYLATING AGENT ON EHRLICH ASCITES CELLS

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Abstract
Based on relatively simple experimental results presented in this report, it appears that the mode of action of a carcinostatic alkylating agent is directly related to its influence on the steady-state level of DPN of tumor cells. Inhibitors of DPNase counteract the glycolysis depressing action of this drug. Isolated DPNase itself is uninfluenced by the carcinostatic agent. The mechanism of intracellular activation of DPNase, presumably due to a loss of intracellular nicotinamide elicited by the carcinostatic agent, as proposed by Hilz et al., is improbable, because the intracellular concentration of nicotinamide (5-9 X 10-5 M) is too low to inhibit DPNase activity.