Sabatier L, Lebeau J, Dutrillaux B
CEA Laboratoire de Cytogénétique, Fontenay aux roses, France.
Int J Radiat Biol. 1994 Nov;66(5):611-3. doi: 10.1080/09553009414551701.
In recent years, evidence has been presented suggesting that genomic instability can appear several generations after cellular exposure to radiations. Kadhim et al. (1992) have shown that irradiation by alpha-particles of Pu238 (LET = 120 keV/microns) induce a transmissible instability in mouse haematopoietic cells. Working with human dermis fibroblasts irradiated by heavy ions in a large range of LETs (386-13,600 keV/microns), we demonstrated that an instability could also be acquired by human cells and that particular chromosomes (13, 16, 1) were recurrently involved in telomeric associations (Sabatier et al. 1992). This instability resulted in specific chromosome imbalances and in a particular monosomy 13 (Martins et al. 1993). In this study, we wanted to determine whether telomeres are shortened with the appearance of the chromosomal instability. Our results show no drastic shortening of the mean length of telomeres by Southern blot. By in situ hybridization we are looking to see if chromosomes specifically involved in instability have alterations of the telomeres. We have observed large variations of the hybridization signal of individual telomeres with no telomeric sequences detectable at the junction of end to end associations.
近年来，已有证据表明，细胞暴露于辐射后，基因组不稳定性可能在几代之后才出现。卡迪姆等人（1992年）已表明，用钚238的α粒子（传能线密度=120 keV/微米）进行照射会在小鼠造血细胞中诱发一种可遗传的不稳定性。我们用一系列传能线密度（386 - 13,600 keV/微米）的重离子照射人真皮成纤维细胞，结果表明人类细胞也可能获得不稳定性，并且特定的染色体（13号、16号、1号）经常参与端粒关联（萨巴蒂埃等人，1992年）。这种不稳定性导致了特定的染色体失衡以及一种特定的13号染色体单体缺失（马丁斯等人，1993年）。在本研究中，我们想确定随着染色体不稳定性的出现，端粒是否会缩短。我们的结果通过Southern印迹法显示端粒平均长度没有急剧缩短。通过原位杂交，我们想看看特别涉及不稳定性的染色体是否有端粒改变。我们观察到单个端粒的杂交信号有很大差异，在端端关联的连接处未检测到端粒序列。
