Weissberg J B, Fischer J J, Moulder J E, Fischer D B
Int J Radiat Oncol Biol Phys. 1984 Jul;10(7):1073-8. doi: 10.1016/0360-3016(84)90180-9.
The effect of the protein synthesis inhibitor cycloheximide (CHM) on normal tissue tolerance and tumor control in the rat following single doses of radiation has been studied. We have previously shown that the drug protects against skin damage when administered prior to irradiation of the hind limbs. It does not protect against six-month lethality when given prior to irradiation of the kidneys. In the present studies protection of rat bone marrow as evidenced by 30-day lethality was observed when CHM was given prior to whole-body irradiation. When CHM was given to rats bearing the BA1112 tumor, it had no protective effect on radiocurability. Therapeutically favorable differential protection of rapidly proliferating normal tissue over tumor can be achieved when CHM is administered prior to single radiation doses in the rat. This effect is most likely due to inhibition of protein synthesis and resultant interruption of the cell cycle in proliferating normal tissue. Further studies are required to determine the clinical applicability of CHM.
研究了蛋白质合成抑制剂环己酰亚胺（CHM）对大鼠单次辐射后正常组织耐受性和肿瘤控制的影响。我们之前已经表明，在照射后肢之前给药，该药物可防止皮肤损伤。在照射肾脏之前给药，它不能防止六个月的致死率。在本研究中，当在全身照射之前给予CHM时，观察到以30天致死率为证据的大鼠骨髓保护作用。当将CHM给予患有BA1112肿瘤的大鼠时，它对放射治愈率没有保护作用。当在大鼠单次辐射剂量之前给予CHM时，可以实现对快速增殖的正常组织优于肿瘤的治疗性有利的差异保护。这种作用最可能是由于蛋白质合成的抑制以及增殖正常组织中细胞周期的中断。需要进一步研究以确定CHM的临床适用性。
