ENHANCEMENT OF MITOGEN-STIMULATED PROLIFERATION OF LOW-DOSE RADIATION-ADAPTED MOUSE SPLENOCYTES

We have monitored mitogen-stimulated mouse splenocyte proliferation as a biological end point of radiation damages to access adaptive respon se to ionizing radiation. When cells were pre-exposed to an adapting d ose of 0. 01 Gy of low dose gamma-ray 4, 7, and 20 hours prior to an a cute challenging dose of 2 Gy, most significant enhancement in splenoc yte proliferation was induced at 4 hour interval. When the challenging high dose was varied, an adaptive response was observed at up to 4 Gy of high dose gamma-ray challenge. Gamma-ray-irradiated mouse splenocy te showed characteristic morphology of apoptotic cells. The extent of DNA fragmentation, another characteristic of apoptotic cells, was also reduced in low dose gamma-ray-adapted cells. The addition of protein of RNA synthesis inhibitor, cycloheximide or 5.6-dichloro-1-beta-d-rib ofuranosylbenzimidazol (DRFB), respectively during adaptation period, the period between low and high dose irradiations, were able to inhibi t the induction of adaptive response. These data suggest that to induc e adaptive response to ionizing radiation in mouse splenocytes, both p rotein and RNA synthesis are required.