The changes in pO2 caused by
nicotinamide in the FSaII mouse
tumor and three different xenografts of human
tumors, HP-56, FaDu, and EO1, grown subcutaneously in the legs of mice were studied. The
tumor pO2, as measured with
microelectrodes, began to rise soon after the host mice were injected intraperitoneally with 500 mg/kg
nicotinamide, and it increased continuously for 100-120 min. The rate and magnitude of the increase in
tumor pO2 was dependent on the
tumor line and also on the
tumor size. In FSaII
tumors, the increase in pO2 caused by
nicotinamide was relatively small in the well-oxygenated small
tumors (173 +/- 5 mm3) compared with that in the larger
tumors (515 +/- 25 mm3). The blood perfusion in FSaII
tumors as measured with the
laser Doppler method was also increased by
nicotinamide. The growth delay in FSaII
tumors induced by X irradiation was enhanced significantly by
nicotinamide. It was concluded that the enhancement of radiation damage in the experimental
tumors in mice by
nicotinamide, as observed in the present study and reported by others, is due to an increase in intratumor pO2, possibly as a result of an increase in blood perfusion.