Kantor G J, Hull D R
Biophys J. 1979 Sep;27(3):359-70. doi: 10.1016/S0006-3495(79)85223-6.
Nondividing human diploid fibroblasts maintained in medium containing 0.5% calf serum do not survive when exposed to low doses of UV (254 nm). The extent of killing is dose and strain dependent. DNA excision repair-proficient cells are more resistant than excision repair-deficient cells. Results of measurements of the effect of UV on RNA and protein synthesis in repair-proficient and -deficient (XP12BE) cells are reported. UV causes an immediate and equal depression of the RNA synthesis rate in both kinds of cells. A recovery to control rates was observed only at low (5 J/m2) doses in repair-deficient cells and at higher doses (20 J/m2) in repair-proficient cells. No recovery was observed at doses that cause substantial reductions in survival (greater than 5 J/m2 for XP12BE; greater than 40 J/m2 for repair-proficient populations). No initial effect on rate of protein synthesis was detected at doses less than 20 J/m2. However, in XP12BE populations, a decreased rate first evident at 15-30 h post-UV and before any cell degeneration and loss was observed for doses as low at 7 J/m2. This delayed effect was not observed in repair-proficient populations. The results are consistent with the hypothesis that the lethal action of UV in nondividing cells is one on DNA that leads to an inhibition of required protein synthesis by preventing RNA transcription.
在含有0.5%小牛血清的培养基中培养的不分裂人类二倍体成纤维细胞,暴露于低剂量紫外线(254纳米)时无法存活。杀伤程度取决于剂量和细胞株。DNA切除修复功能正常的细胞比切除修复功能缺陷的细胞更具抗性。本文报告了紫外线对修复功能正常和缺陷(XP12BE)细胞中RNA和蛋白质合成影响的测量结果。紫外线会使两种细胞中的RNA合成速率立即且同等程度地降低。仅在修复缺陷细胞中低剂量(5 J/m²)时以及修复功能正常细胞中高剂量(20 J/m²)时观察到RNA合成速率恢复到对照水平。在导致存活率大幅降低的剂量下(XP12BE细胞大于5 J/m²;修复功能正常细胞群体大于40 J/m²)未观察到恢复现象。在小于20 J/m²的剂量下未检测到对蛋白质合成速率的初始影响。然而,在XP12BE细胞群体中,在紫外线照射后15 - 30小时首次明显出现速率降低,且在低至7 J/m²的剂量下在任何细胞退化和损失出现之前就已观察到这种情况。在修复功能正常的细胞群体中未观察到这种延迟效应。这些结果与以下假设一致:紫外线在不分裂细胞中的致死作用是作用于DNA,通过阻止RNA转录导致所需蛋白质合成受到抑制。