Ritter Sylvia, Nasonova Elena, Furusawa Yoshiya, Ando Koichi
Biophysik, GSI, 64291 Darmstadt, Germany.
J Radiat Res. 2002 Dec;43 Suppl:S175-9. doi: 10.1269/jrr.43.s175.
The time-course of Fe-ion (200 MeV/u, 440 keV/microm) and X-ray induced chromosomal damage was investigated in human lymphocytes. After cells were exposed in G0 and stimulated to grow, aberrations were measured in first-cycle metaphases harvested 48, 60 and 72 h post-irradiation. Additionally, lesions were analysed in G2 and mitotic (M) cells collected at 48 h using calyculin A-induced premature chromosome condensation (PCC). Following X-irradiation, similar aberration yields were found in all of the samples scored. In contrast, after Fe-ion exposure a drastic increase in the aberration frequency with sampling time was observed, i.e. cells arriving late at the first mitosis carried more aberrations than those arriving at earlier times. The PCC data indicate that the delayed entry of heavily damaged cells into mitosis observed after Fe-ion irradiation resulted from a prolonged arrest in G2. Altogether these experiments provide further evidence that in the case of high-LET exposure cell-cycle delays of severely damaged cells have to be taken into account for any meaningful quantification of chromosomal damage and, consequently, for an accurate estimate of the RBE.
在人类淋巴细胞中研究了铁离子（200 MeV/u，440 keV/微米）和X射线诱导的染色体损伤的时间进程。细胞在G0期暴露后被刺激生长，在照射后48、60和72小时收获的第一周期中期相中测量畸变。此外，使用花萼海绵诱癌素A诱导的早熟染色体凝缩（PCC），对在48小时收集的G2期和有丝分裂（M）期细胞中的损伤进行分析。X射线照射后，在所有评分样本中发现了相似的畸变产额。相比之下，铁离子暴露后，观察到畸变频率随取样时间急剧增加，即较晚进入第一次有丝分裂的细胞比较早进入的细胞携带更多的畸变。PCC数据表明，铁离子照射后观察到的严重受损细胞进入有丝分裂的延迟是由于G2期的延长停滞。总之，这些实验进一步证明，在高传能线密度照射的情况下，对于任何有意义地量化染色体损伤，进而准确估计相对生物效应，都必须考虑严重受损细胞的细胞周期延迟。
