Denisenko M F, Soldatenkov V A, Belovskaya L N, Filippovich I V
Institute of Biophysics, U.S.S.R. Department of Health, Moscow.
Int J Radiat Biol. 1989 Sep;56(3):277-85. doi: 10.1080/09553008914551441.
Agents that induce DNA strand breaks evoke a drop in the NAD content in mouse thymocytes. A decrease in the endogenous NAD content that occurs immediately after gamma-irradiation of thymocytes is entirely attributed to the activation of poly(ADP-ribosylation). The addition of 5 mM benzamide before irradiation prevents the postirradiation drop of the NAD level but has no effect on chromatin degradation and cell death. In contrast to liver nuclei, pre-incubation of mouse thymic nuclei with NAD had no effect on the subsequent chromatin endonucleolysis by Ca2+/Mg2+-dependent endonuclease. It is suggested that the NAD-poly(ADP-ribose) polymerase system is probably not the trigger in the radiation-induced programmed death of mouse thymocytes, but may merely be indicative of the radiation response of these cells.
诱导DNA链断裂的试剂会导致小鼠胸腺细胞中烟酰胺腺嘌呤二核苷酸（NAD）含量下降。胸腺细胞经γ射线照射后立即出现的内源性NAD含量降低完全归因于多聚（ADP-核糖基化）的激活。照射前添加5 mM苯甲酰胺可防止照射后NAD水平下降，但对染色质降解和细胞死亡没有影响。与肝细胞核不同，用NAD预孵育小鼠胸腺细胞核对随后由Ca2+/Mg2+依赖性核酸内切酶引起的染色质内切核酸酶作用没有影响。有人提出，NAD-多聚（ADP-核糖）聚合酶系统可能不是辐射诱导的小鼠胸腺细胞程序性死亡的触发因素，而可能仅仅是这些细胞辐射反应的一个指标。
