Miyakoshi J, Oda W, Inagaki C
Radiat Res. 1985 Jun;102(3):359-66.
The modifying effects of m-aminobenzamide (m-ABA), an inhibitor of poly(ADP-ribose) synthesis, on 42 degrees C hyperthermia- and/or radiation-induced cell killing were examined in Chinese hamster V-79 cells. When cells were exposed to 42 degrees C hyperthermia in combination with m-ABA (10 mM), cell survival decreased compared with that for 42 degrees C hyperthermia alone. Thermosensitizing effects of m-ABA changed with treatments in a decreasing order of during and after heating greater than during heating greater than after heating. Treatments with m-ABA during and/or after X irradiation enhanced radiation-induced cell killing. When cells were exposed to combined treatment with X irradiation, 42 degrees C hyperthermia (60 min), and m-ABA (24 hr), cell survival decreased markedly compared with that for X irradiation alone. However, with both X----42 degrees C and X----42 degrees C----m-ABA, the enhancement ratios (ER), designated as D0 ratio, were similar. These results suggest that the mechanisms of radiosensitization by m-ABA may be similar to those of 42 degrees C hyperthermia.
研究了聚（ADP - 核糖）合成抑制剂间氨基苯甲酰胺（m - ABA）对中国仓鼠V - 79细胞在42℃高温和/或辐射诱导的细胞杀伤中的修饰作用。当细胞暴露于42℃高温并联合m - ABA（10 mM）时，与单独42℃高温处理相比，细胞存活率降低。m - ABA的热敏化作用随处理方式而变化，其顺序为加热期间和加热后大于加热期间大于加热后。在X射线照射期间和/或之后用m - ABA处理可增强辐射诱导的细胞杀伤。当细胞接受X射线照射、42℃高温（60分钟）和m - ABA（24小时）联合处理时，与单独X射线照射相比，细胞存活率显著降低。然而，对于X→42℃和X→42℃→m - ABA两种处理方式，指定为D0比的增强率（ER）相似。这些结果表明，m - ABA的放射增敏机制可能与42℃高温的机制相似。
