Holmberg M, Gumauskas E
National Institute of Radiation Protection, Stockholm, Sweden.
Mutat Res. 1990 Oct;232(2):261-6. doi: 10.1016/0027-5107(90)90132-n.
Human lymphocytes in the quiescent stage were UVC-irradiated and then incubated for 90 min in the presence of the DNA-repair inhibitor ara-C. The cells were then cultured and analyzed for chromosome aberrations. A single treatment with UVC or ara-C gives rise to a very low yield of dicentrics, whereas the combined treatment can induce a high frequency of these chromosome-type aberrations. The yield in the combined treatment is approximately proportional to the square of the UVC fluence in the range 1-3 J/m2. In addition, the experiments demonstrate that synergistic effects arise when cells are treated with UVC + ara-C and then exposed to X-rays. The results can be explained on the assumption that the UVC + ara-C treatment induces DNA double-strand breaks which, to the first approximation, are randomly distributed over the chromosomes. These breaks are able to interact with each other as well as with X-ray-induced DNA double-strand breaks to form a chromosome-type exchange aberration.
将处于静止期的人类淋巴细胞进行紫外线C（UVC）照射，然后在DNA修复抑制剂阿糖胞苷（ara-C）存在的情况下孵育90分钟。接着对细胞进行培养并分析染色体畸变情况。单独用UVC或ara-C处理只会产生极低频率的双着丝粒，而联合处理则可诱导出高频率的这类染色体型畸变。在1 - 3 J/m2范围内，联合处理中的畸变率大致与UVC通量的平方成正比。此外，实验表明，当细胞先用UVC + ara-C处理然后再暴露于X射线时会产生协同效应。这些结果可以基于这样的假设来解释：UVC + ara-C处理会诱导DNA双链断裂，初步看来，这些断裂在染色体上是随机分布的。这些断裂能够相互作用，也能与X射线诱导的DNA双链断裂相互作用，从而形成染色体型交换畸变。
