Yasui L S, Hofer K G
Int J Radiat Biol Relat Stud Phys Chem Med. 1986 Apr;49(4):601-10. doi: 10.1080/09553008514552851.
The role of mitochondrial DNA in radiation-induced cell death was determined by selective [125I]iododeoxyuridine (125IUdR) incorporation into exclusively nuclear sites compared to labelling in both nuclear and mitochondrial DNA of Chinese hamster cells. Such selectivity was achieved by using berenil (25 micrograms/ml for 24 h), a drug which inhibits mitochondrial DNA synthesis without affecting incorporation of 125IUdR into nuclear DNA but does not result in reduced clonogenicity or cell cycle perturbations or alteration in the X-ray response of cells. There was no difference in cell killing between cells with nuclear labelling alone compared with nuclear plus mitochondrial labelling. The absence of decays in mitochondrial DNA does not affect the ability of 125I to induce lethal cell damage. The two treatment groups have superimposable curves with a D0 of 96 decays/cell. These findings indicate that mitochondrial DNA is not the most sensitive target for radiation-induced cell death from 125I decay.
通过将[125I]碘脱氧尿苷（125IUdR）选择性掺入中国仓鼠细胞的细胞核位点，并与同时标记细胞核和线粒体DNA的情况进行比较，确定了线粒体DNA在辐射诱导的细胞死亡中的作用。这种选择性是通过使用贝尼尔（25微克/毫升，处理24小时）实现的，该药物可抑制线粒体DNA合成，而不影响125IUdR掺入细胞核DNA，但不会导致克隆形成能力降低、细胞周期紊乱或细胞对X射线反应的改变。仅细胞核标记的细胞与细胞核加线粒体标记的细胞在细胞杀伤方面没有差异。线粒体DNA中不存在衰变并不影响125I诱导致死性细胞损伤的能力。两个处理组的存活曲线相互重叠，D0为96次衰变/细胞。这些发现表明，线粒体DNA不是125I衰变诱导细胞死亡的最敏感靶点。
