Sellins K S, Cohen J J
Department of Microbiology and Immunology, University of Colorado School of Medicine, Denver 80262.
Radiat Res. 1991 Apr;126(1):88-95.
Mild hyperthermia (43 degrees C for 1 h) induces extensive double-stranded DNA fragmentation and, at a later time, cell death in murine thymocytes. The cleavage of DNA into oligonucleosome-sized fragments resembles that observed in examples of apoptosis including radiation-induced death of thymocytes. Following hyperthermia, incubation at 37 degrees C is necessary to detect DNA fragmentation, although protein and RNA synthesis do not seem to be required. Two protein synthesis inhibitors, cycloheximide and emetine, and two RNA synthesis inhibitors, actinomycin D and 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole, do not inhibit DNA fragmentation or cell death in heated thymocytes at concentrations which significantly block these effects in irradiated thymocytes. We have used this difference in sensitivity to show that the DNA fragmentation induced in thymocytes which are irradiated and then heated seems to be caused only by the heating and not by the irradiation.
轻度热疗(43摄氏度,持续1小时)可诱导小鼠胸腺细胞出现广泛的双链DNA断裂,随后导致细胞死亡。DNA被切割成寡核小体大小的片段,这与在包括辐射诱导的胸腺细胞死亡在内的凋亡实例中观察到的情况相似。热疗后,需要在37摄氏度孵育以检测DNA断裂,尽管似乎不需要蛋白质和RNA合成。两种蛋白质合成抑制剂,放线菌酮和依米丁,以及两种RNA合成抑制剂,放线菌素D和5,6 - 二氯 - 1 - β - D - 呋喃核糖基苯并咪唑,在能显著阻断辐射胸腺细胞中这些效应的浓度下,并不抑制热疗胸腺细胞中的DNA断裂或细胞死亡。我们利用这种敏感性差异表明,先接受辐射然后再加热的胸腺细胞中诱导的DNA断裂似乎仅由加热引起,而非辐射所致。