Kondo T, Ueda K, Kano E
Department of Radiation Biophysics, Kobe University School of Medicine, Japan.
Anticancer Res. 1995 Jan-Feb;15(1):83-6.
The interaction between hyperthermia and a DNA topoisomerase I inhibitor, 7-ethyl-10-(4-(1-piperidyl)-1-piperidyl)-carbonyloxy- camptothecin (CPT-11), was studied in the mouse mammary carcinoma FM3A cells. When the cells were treated with CPT-11 at a concentration of 5 micrograms/ml and 44 degrees C hyperthermia for 60 min, an enhancement of formation of single stand breaks (ssb) of DNA was observed. However, a decrease of ssb was observed when hyperthermia was combined with CPT-11 at 50 micrograms/ml. For inhibition of DNA synthesis additive effects were observed for treatment with CPT-11 at 5 micrograms/ml combined with hyperthermia. On the other hand, protective effects were observed for the combined treatment at 50 micrograms/ml. These results indicate that the hyperthermic modification of the effect of CPT-11 on the induction of DNA damage was diverse at low or high concentrations.
在小鼠乳腺癌FM3A细胞中研究了热疗与DNA拓扑异构酶I抑制剂7-乙基-10-(4-(1-哌啶基)-1-哌啶基)-羰基氧喜树碱（CPT-11）之间的相互作用。当细胞用浓度为5微克/毫升的CPT-11处理并在44℃热疗60分钟时，观察到DNA单链断裂（ssb）形成增加。然而，当热疗与50微克/毫升的CPT-11联合使用时，观察到ssb减少。对于DNA合成抑制，在5微克/毫升的CPT-11与热疗联合处理时观察到相加效应。另一方面，在50微克/毫升的联合处理中观察到保护作用。这些结果表明，CPT-11对DNA损伤诱导作用的热疗修饰在低浓度或高浓度下是不同的。
