Rosenstein B S
Department of Radiation Medicine, Brown University, Providence, RI 02912.
Int J Radiat Biol. 1989 Aug;56(2):131-8. doi: 10.1080/09553008914551281.
Cultures of the solar UV-sensitive cell lines, DRP 36 and DRP 153, and of the parental ICR 2A cell line, were exposed to 150 kJ/m2 of sunlamp UV greater than 315 nm plus photoreactivating light. This treatment resulted in the induction primarily of non-dimer DNA damage. Following either a 0, 3, 6, 12 or 24 h incubation, the cultures were pulse-labelled with [3H]thymidine, and the synthesis of different size classes of replicon intermediates measured using the alkaline step elution assay. For all three cell lines tested, an immediate depression of low molecular weight DNA synthesis was observed. This was followed by an inhibition of all size classes of replicon intermediates. Within 12 h following irradiation, recovery of DNA synthesis was observed, which was generally most apparent for low molecular weight DNA. The ICR 2A cells exhibited a nearly full recovery in all size classes of DNA synthesized by 24 h. However, a much smaller recovery of DNA synthesis was detected for the DRP 36 and DRP 153 cultures. This continued inhibition was primarily in the synthesis of full replicon size DNA, and was most pronounced for the DRP 36 cells. Hence, it appears that replicon chain elongation continues to be inhibited in these solar UV-sensitive cell lines long after irradiation.
将对紫外线敏感的细胞系DRP 36和DRP 153以及亲本ICR 2A细胞系进行培养,使其暴露于大于315 nm的150 kJ/m²的太阳灯紫外线及光复活光下。这种处理主要导致非二聚体DNA损伤的诱导。在0、3、6、12或24小时的孵育后,用[³H]胸腺嘧啶核苷对培养物进行脉冲标记,并使用碱性逐步洗脱分析法测量不同大小类别的复制子中间体的合成。对于所有测试的三种细胞系,均观察到低分子量DNA合成立即受到抑制。随后所有大小类别的复制子中间体均受到抑制。在照射后12小时内,观察到DNA合成的恢复,这在低分子量DNA中通常最为明显。ICR 2A细胞在24小时内合成的所有大小类别的DNA中均表现出几乎完全的恢复。然而,对于DRP 36和DRP 153培养物,检测到的DNA合成恢复要小得多。这种持续的抑制主要在于完整复制子大小DNA的合成,并且在DRP 36细胞中最为明显。因此,在这些对太阳紫外线敏感的细胞系中,照射后很长时间复制子链的延伸似乎仍受到抑制。