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 response to ionizing radiation. When cells were pre-exposed to an adapting dose of 0. 01 Gy of low dose gamma-ray 4, 7, and 20 hours prior to an acute challenging dose of 2 Gy, most significant enhancement in splenocyte 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 splenocyte 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 or RNA synthesis inhibitor, cycloheximide or 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazol (DRFB), respectively during adaptation period, the period between low and high dose irradiations, were able to inhibit the induction of adaptive response. These data suggest that to induce adaptive response to ionizing radiation in mouse splenocytes, both protein and RNA synthesis are required.
Hyun
S J
SJ
Department of Chemistry, Hanyang University, Korea.
Yoon
M Y
MY
Kim
T H
TH
Kim
J H
JH
D000818:Animals; D017209:Apoptosis / Q000528:radiation effects; D002455:Cell Division / Q000528:radiation effects; D004249:DNA Damage; D005720:Gamma Rays; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis; D013154:Spleen / Q000166:cytology / Q000528:radiation effects*
D012313:RNA