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首页> 外文期刊>Radiation Research: Official Organ of the Radiation Research Society >INSULIN AND INSULIN-LIKE GROWTH FACTOR-1 (IGF-1) INHIBIT REPAIR OF POTENTIALLY LETHAL RADIATION DAMAGE AND CHROMOSOME ABERRATIONS AND ALTER DNA REPAIR KINETICS IN PLATEAU-PHASE A549 CELLS
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INSULIN AND INSULIN-LIKE GROWTH FACTOR-1 (IGF-1) INHIBIT REPAIR OF POTENTIALLY LETHAL RADIATION DAMAGE AND CHROMOSOME ABERRATIONS AND ALTER DNA REPAIR KINETICS IN PLATEAU-PHASE A549 CELLS

机译：胰岛素和类胰岛素生长因子-1（IGF-1）抑制高原阶段A549细胞潜在的致命性辐射损伤和染色体异常以及DNA修复动力学。

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Plateau-phase A549 cells exhibit a high capacity for repair of potentially lethal radiation damage (PLD) when allowed to recover in their own spent medium. Addition of either insulin or insulin-like growth factor-1 (IGF-1) to the spent medium 60 to 120 min before irradiation significantly inhibits PLD repair. The 9-h recovery factor (survival with holding/survival without holding) is reduced from 10.8 +/- 0.7 to 3.4 +/- 0.3 by insulin and to 3.0 +/- 0.4 by IGF-1. Neither growth factor alters the cell age distribution of the plateau-phase cells, increases the rate of incorporation of 5-bromo-2'-deoxyuridine into DNA, or alters the extent of radiation-induced mitotic delay in cells subcultured immediately after irradiation. Both insulin and IGF-1 alter the kinetics for rejoining of DNA double-strand breaks (DSBs), slowing the fast component of rejoining significantly, However, these growth factors have no effect on the initial level of DSBs or on the percentage of residual unrejoined breaks at 120 min postirradiation. Both growth factors affect repair of lesions leading to dicentric, but not to acentric, chromosome aberrations significantly. In control cells (treated with phosphate-buffered saline, 90 min prior to irradiation), the half-time for disappearance of dicentrics was 4.1 h (3.4 to 5.1 h), and 47.1 +/- 3.7% of the residual damage remained at 24 h postirradiation. Insulin and IGF-1 increased the half-time for disappearance of dicentrics to 5.2 h (3.9 to 7.7 h) and 5.7 h (5.5 to 5.9 h), respectively, and increased residual damage to 56.1 +/- 5.9% and 60.8 +/- 6.0%, respectively. Overall, these data show that insulin and IGF-1 inhibit PLD repair in A549 cells by mechanisms which are independent of changes in cell cycle parameters. The data suggest that the growth factors act by inducing changes in chromatin conformation which promote misrepair of radiation-damaged DNA. (C) 1995 by Radiation Research Society [References: 44]
机译：当允许在其自己用过的培养基中恢复时，高原期A549细胞具有修复潜在致命辐射损伤（PLD）的高能力。在辐照前60至120分钟，将胰岛素或胰岛素样生长因子-1（IGF-1）添加到用过的培养基中会显着抑制PLD修复。 9小时恢复因子（有保留的生存率/无保留的生存率）通过胰岛素从10.8 +/- 0.7降低到3.4 +/- 0.3，而通过IGF-1降低到3.0 +/- 0.4。两种生长因子均不会改变平台期细胞的细胞年龄分布，也不会提高5-溴-2'-脱氧尿苷掺入DNA的速率，也不会改变辐射后立即继代培养的细胞中辐射诱导的有丝分裂延迟的程度。胰岛素和IGF-1都改变了DNA双链断裂（DSB）重新结合的动力学，显着减慢了重新结合的快速成分。但是，这些生长因子对DSB的初始水平或未结合残基的百分比没有影响。照射后120分钟时破裂。两种生长因子都影响修复的修复，从而导致双着丝粒而不是无着丝粒的染色体畸变。在对照细胞中（在照射前90分钟，用磷酸盐缓冲盐水处理），双着丝粒消失的半衰期为4.1小时（3.4至5.1小时），而剩余损伤的47.1 +/- 3.7％保留在24 h照射后。胰岛素和IGF-1将双着丝粒消失的半衰期分别增加至5.2小时（3.9至7.7小时）和5.7小时（5.5至5.9小时），并将残余损伤增加至56.1 +/- 5.9％和60.8 + / -分别为6.0％。总的来说，这些数据表明胰岛素和IGF-1通过独立于细胞周期参数变化的机制抑制A549细胞中的PLD修复。数据表明，生长因子通过诱导染色质构象变化而起作用，从而促进放射损伤的DNA的错误修复。 （C）1995年，由放射研究学会[参考文献：44]

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