Competition of sodium salt of 9-oxo-10-acridineacetic acid with analogs during induction of interferon in the mouse bone marrow-derived macrophages.

Analogs of 9-oxo-10-acridineacetic acid (CMA) including new synthetic compounds, were found to be valuable tools for investigating the mechanism of interferon (IFN) induction. Experiments were performed on the long-term cultures of mouse bone marrow-derived macrophages which are unusually susceptible to IFN induction by CMA. CMA in the optimal nontoxic concentration of 600 micrograms/ml may induce in the macrophages up to 3.500 units of IFN/ml. The response was found to be dose related. The analogs of CMA, compounds 3, 7-16, were found to be inactive as IFN inducers. However, the analogs 3, and 8-16 administered together with the suboptimal doses of CMA enhanced by 10 to 40-fold the interferon response to CMA. On the other hand, the compound 7 was shown to inhibit completely the induction of interferon by CMA. L-tryptophan was inactive as either enhancer or inhibitor of CMA. The mode of action of CMA is explained in terms of the hormonal concept of IFN induction.