Nagasawa H, Little J B
Mutat Res. 1983 May;109(2):297-308. doi: 10.1016/0027-5107(83)90054-4.
Survival, cumulative labeling indices and chromosomal aberrations were studied in normal, ataxia telangiectasia (AT) and hereditary retinoblastoma fibroblasts after X-irradiation during density-inhibition of growth and immediate release by subculture to low density. The D0 of the survival curves were: normal strains, 150-160 rad; Retinoblastoma strains AG 1880, 95 rad; AG 1978, 40-50 rad (sensitive fraction); AT5BI, 45 rad. Mainly chromosome-type Aberrations were induced in normal and retinoblastoma cells. The frequency of X-ray-induced chromosomal aberrations was much higher in AT5BI cells, and 33-45% were of the chromatid type. Normal and retinoblastoma cells showed a measureable X-ray induced G1 delay before entering S. In addition, a fraction of the cells showed an apparently irreversible G1 block; these cells did not initiate DNA synthesis up to 120 h post-irradiation and subculture. The G1 block was much more marked in retinoblastoma cells; after 400 rad about 70% of retinoblastoma cells did not enter S as compared with only 20% of normal cells. Neither a G1 delay nor a G1 block was observed in AT cells irradiated with up to 400 rad despite their hypersensitivity to cell killing by X-rays and evidence of severe chromosome damage. These results suggest different mechanisms for the X-ray hypersensitivity of AT and retinoblastoma cells.
研究了正常、共济失调毛细血管扩张症（AT）和遗传性视网膜母细胞瘤成纤维细胞在生长密度抑制期间经X射线照射后以及通过传代培养至低密度立即释放后的存活率、累积标记指数和染色体畸变情况。存活曲线的D0值分别为：正常菌株150 - 160拉德；视网膜母细胞瘤菌株AG 1880为95拉德；AG 1978为40 - 50拉德（敏感部分）；AT5BI为45拉德。正常细胞和视网膜母细胞瘤细胞主要诱导产生染色体型畸变。X射线诱导的染色体畸变频率在AT5BI细胞中要高得多，且33 - 45%为染色单体型。正常细胞和视网膜母细胞瘤细胞在进入S期之前显示出可测量的X射线诱导的G1期延迟。此外，一部分细胞显示出明显不可逆的G1期阻滞；这些细胞在照射和传代培养后长达120小时都未启动DNA合成。视网膜母细胞瘤细胞中的G1期阻滞更为明显；400拉德照射后，约70%的视网膜母细胞瘤细胞未进入S期，而正常细胞只有20%。尽管AT细胞对X射线杀伤超敏且有严重染色体损伤的证据，但照射剂量高达400拉德时未观察到G1期延迟或G1期阻滞。这些结果提示AT细胞和视网膜母细胞瘤细胞对X射线超敏存在不同机制。
