Peng Yuanlin, Borak Thomas B, Bouffler Simon D, Ullrich Robert L, Weil Michael M, Bedford Joel S
Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523, USA.
Radiat Res. 2009 Apr;171(4):484-93. doi: 10.1667/RR1548.1.
Chromosome aberrations in mitotic bone marrow cells of CBA/Ca and C57BL/6 mice were measured 1 day after exposure to 1 Gy of 1 GeV/nucleon 56Fe ions or 3 Gy of gamma rays. The proportion that have lost a region of chromosome 2 containing the PU.1 gene could be explained by a model based on these measurements. The distribution of aberrations among cells was close to the expected Poisson for the gamma-irradiated cells, but for the HZE 56Fe ions the distribution was highly dispersed. The observations were consistent with the results of an analysis similar to that of Edwards and co-workers in 1980 after ex vivo irradiation of human blood with alpha particles. The analysis used to fit the current data was based on a compound Poisson process, also used previously by others, but in addition included the random nature of parameters involved such as cell nuclear diameter, particle traversal lengths through cell nuclei, production of aberrations, and cell cycle arrest per traversal. From the measured numbers of acentric fragments produced, the relative size of chromosome 2 and the region associated with PU.1 deletions, an independent prediction of PU.1 loss agreed well with measurements described in the accompanying paper.
在CBA/Ca和C57BL/6小鼠的有丝分裂骨髓细胞中，于暴露于1 Gy的1 GeV/核子56Fe离子或3 Gy的γ射线后1天测量染色体畸变。丢失包含PU.1基因的2号染色体区域的比例可以用基于这些测量结果的模型来解释。γ射线照射细胞的畸变在细胞间的分布接近预期的泊松分布，但对于高电荷态56Fe离子，分布高度分散。这些观察结果与1980年爱德华兹及其同事在用α粒子对人体血液进行离体照射后的分析结果一致。用于拟合当前数据的分析基于复合泊松过程，其他人之前也使用过，但此外还包括了诸如细胞核直径、粒子穿过细胞核的长度、畸变产生以及每次穿过时细胞周期停滞等相关参数的随机性。根据所测量的无着丝粒片段数量、2号染色体的相对大小以及与PU.1缺失相关的区域，对PU.1缺失的独立预测与随附论文中描述的测量结果吻合良好。
