肿瘤启动子、蛋白酶抑制剂和修复过程对小鼠细胞中X射线诱导的姐妹染色单体交换的影响。
Effect of tumor promoters, protease inhibitors, and repair processes on x-ray-induced sister chromatid exchanges in mouse cells.
作者信息
Nagasawa H, Little J B
出版信息
Proc Natl Acad Sci U S A. 1979 Apr;76(4):1943-7. doi: 10.1073/pnas.76.4.1943.
The induction of sister chromatid exchanges (SCE) in the second postirradiation mitosis was studied in mouse 10T1/2 cells irradiated with 400 rads (4 grays) and maintained in stationary growth for several hours after x-ray exposure (similar to liquid holding recovery experiments in bacterial cells). X-irradiation with no recovery period induced few SCE. With short recovery intervals, however, the SCE frequency rose in parallel with the increase in survival, reaching a maximum increase of 2-fold after 4 hr; SCE declined with longer recovery intervals. The influence of postirradiation incubation with the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) and with the protease inhibitors antipain and leupeptin was studied on spontaneous, x-ray-induced (no recovery), and recovery-induced (4 hr) SCE. TPA (0.1 microgram/ml and 1.0 microgram/ml) increased the frequency of both spontaneous and direct x-ray-induced SCE, but not of recovery-induced SCE. Incubation with the protease inhibitors suppressed both TPA- and recovery-induced SCE, but had no effect on direct x-ray-induced SCE. These results are discussed in relation to the hypothesis that promotional events in carcinogenesis may involve the expression of mutational damage in cells by mitotic segregation.
研究了用400拉德（4戈瑞）照射的小鼠10T1/2细胞在第二次辐射后有丝分裂中姐妹染色单体交换（SCE）的诱导情况，并且在X射线照射后让细胞处于静止生长状态数小时（类似于细菌细胞中的液体保留恢复实验）。未经过恢复期的X射线照射诱导出的SCE很少。然而，在短的恢复期后，SCE频率随着存活率的增加而平行上升，在4小时后达到最大增幅2倍；随着恢复期延长，SCE下降。研究了用肿瘤启动子12-O-十四烷酰佛波醇13-乙酸酯（TPA）以及蛋白酶抑制剂抗蛋白酶和亮抑蛋白酶肽进行照射后孵育对自发的、X射线诱导的（无恢复）以及恢复诱导的（4小时）SCE的影响。TPA（0.1微克/毫升和1.0微克/毫升）增加了自发的和直接X射线诱导的SCE频率，但对恢复诱导的SCE没有影响。用蛋白酶抑制剂孵育可抑制TPA诱导的和恢复诱导的SCE，但对直接X射线诱导的SCE没有影响。结合致癌作用中的促进事件可能涉及通过有丝分裂分离在细胞中表达突变损伤这一假说对这些结果进行了讨论。
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