de Laat A, Kroon E D, de Gruijl F R
Department of Dermatology, University Hospital Utrecht, Utrecht University, The Netherlands.
Photochem Photobiol. 1997 Apr;65(4):730-5. doi: 10.1111/j.1751-1097.1997.tb01917.x.
Ultraviolet A (UVA, 315-400 nm) radiation is known to be a complete carcinogen, but in contrast to UVB (280-315 nm) radiation, much of the cell damage is oxygen dependent (mediated through reactive oxygen species), and the dominant premutational DNA lesion(s) remains to be identified. To investigate further the basic differences in UVA and UVB carcinogenesis, we compared in vivo cellular responses, viz. cell cycle progression and transient p53 expression in the epidermis, after UVA1 (340-400 nm) exposure with those after broadband UVB exposure of hairless mice. Using flow cytometry we found a temporary suppression of bromodeoxyuridine (BrdU) uptake in S-phase cells both after UVB and UVA1 irradiation, which only in the case of UVB is followed by an increase to well over control levels. With equally erythemogenic doses (1-2 MED), the modulation of BrdU uptake was more profound after UVB than after UVA1 irradiation. Also, a marked transient increase in the percentage of S-phase cells occurred both after UVB and after UVA1 irradiation, but this increase evolved more rapidly after UVA1 irradiation. Further, p53 expression increased both after UVB and UVA1 irradiations, with peak expression already occurring from 12 to 24 h after UVA1 exposure and around 24 h after UVB exposure. Overall, UVA1 radiation appears to have less of an impact on the cell cycle than UVB radiation, as measured by the magnitude and duration of changes in DNA synthesis and cells in S phase. These differences are likely to reflect basic differences between UVB and UVA1 in genotoxicity and carcinogenic action.
已知紫外线A（UVA，315 - 400纳米）辐射是一种完全致癌物，但与紫外线B（UVB，280 - 315纳米）辐射不同的是，许多细胞损伤是氧依赖性的（通过活性氧介导），并且主要的致突变前DNA损伤仍有待确定。为了进一步研究UVA和UVB致癌作用的基本差异，我们比较了无毛小鼠在接受UVA1（340 - 400纳米）照射和宽带UVB照射后，表皮中的体内细胞反应，即细胞周期进程和瞬时p53表达。通过流式细胞术，我们发现UVB和UVA1照射后，S期细胞中溴脱氧尿苷（BrdU）摄取均出现暂时抑制，只有在UVB照射的情况下，随后会增加到远高于对照水平。在同等红斑剂量（1 - 2最小红斑量）下，UVB照射后BrdU摄取的调节比UVA1照射后更显著。此外，UVB和UVA1照射后，S期细胞百分比均出现明显的瞬时增加，但这种增加在UVA1照射后发展得更快。此外，UVB和UVA1照射后p53表达均增加，UVA1照射后12至24小时以及UVB照射后约24小时出现表达峰值。总体而言，以DNA合成和S期细胞变化的幅度和持续时间来衡量，UVA1辐射对细胞周期的影响似乎比UVB辐射小。这些差异可能反映了UVB和UVA1在遗传毒性和致癌作用方面的基本差异。
