Lee I, Song C W
University of Minnesota Medical School, Department of Therapeutic Radiology, Minneapolis 55455.
Radiat Res. 1992 Apr;130(1):65-71.
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.
研究了烟酰胺对FSaII小鼠肿瘤以及三种不同的人肿瘤异种移植瘤(HP - 56、FaDu和EO1)pO₂的影响,这些肿瘤在小鼠腿部皮下生长。用微电极测量肿瘤pO₂,在宿主小鼠腹腔注射500 mg/kg烟酰胺后不久,肿瘤pO₂开始升高,并持续增加100 - 120分钟。肿瘤pO₂升高的速率和幅度取决于肿瘤类型以及肿瘤大小。在FSaII肿瘤中,与较大肿瘤(515±25 mm³)相比,在氧合良好的小肿瘤(173±5 mm³)中,烟酰胺引起的pO₂升高相对较小。用激光多普勒法测量,FSaII肿瘤中的血液灌注也因烟酰胺而增加。烟酰胺显著增强了X射线照射诱导的FSaII肿瘤的生长延迟。得出结论,如本研究及其他研究报道,烟酰胺增强小鼠实验性肿瘤的辐射损伤是由于肿瘤内pO₂升高,这可能是血液灌注增加的结果。