Blakely E A, Chang P Y, Lommel L
Radiat Res Suppl. 1985;8:S145-57.
The cell-cycle-dependent capacity of synchronized G1-phase human T-1 cells to repair damage from either 425 MeV/u Bragg peak neon ions or 225 kVp X rays has been compared. The dose-survival response to each radiation was measured at early (1.5 h), mid (3.0 h), and late (4.5 h) times after mitotic selection. In addition the age response was characterized by irradiating cell populations at seven ages between 1.5 and 6.0 h after mitosis with single doses of either radiation. Repair of potentially lethal damage (PLDR) was evaluated in both the dose-survival and age-response experiments by holding irradiated cultures at 37 degrees C for 6 h in PBS or PBS containing 60 microM of the DNA polymerase inhibitor 1-beta-D-arabinofuranosyladenine (beta-araA) before trypsinization and plating. Delayed plating showed significant PLDR at all ages irradiated with X rays, with up to 10-fold increases of survival depending on the dose and the cell age at irradiation. There was negligible PLDR after neon-ion exposures to early and mid G1-phase cells; only late G1-phase cells repaired neon damage. The beta-araA treatment after X rays reduced the shoulder of the survival curves at all G1 ages studied, and in early and mid G1 reduced survival below the immediately plated control. beta-araA similarly reduced repair of PLD where it was measurable after neon ions. Differences between low- and high-LET radiation damage and repair are discussed.
已比较了同步化的G1期人T-1细胞修复425 MeV/u布拉格峰氖离子或225 kVp X射线损伤的细胞周期依赖性能力。在有丝分裂选择后的早期(1.5小时)、中期(3.0小时)和晚期(4.5小时)测量了对每种辐射的剂量存活反应。此外,通过用单剂量的任何一种辐射照射有丝分裂后1.5至6.0小时之间七个年龄的细胞群体来表征年龄反应。在剂量存活和年龄反应实验中,通过在胰蛋白酶消化和接种前将照射后的培养物在37℃下于PBS或含有60 microM DNA聚合酶抑制剂1-β-D-阿拉伯呋喃糖基腺嘌呤(β-araA)的PBS中保持6小时来评估潜在致死损伤(PLDR)的修复。延迟接种显示,在用X射线照射的所有年龄中都有显著的PLDR,根据剂量和照射时的细胞年龄,存活率可提高多达10倍。氖离子暴露于早期和中期G1期细胞后PLDR可忽略不计;只有晚期G1期细胞能修复氖损伤。X射线照射后的β-araA处理降低了所有研究的G1年龄下存活曲线的肩部,并且在早期和中期G1期降低了存活率至低于立即接种的对照。β-araA同样降低了氖离子后可测量的PLD的修复。讨论了低LET和高LET辐射损伤及修复之间的差异。