Roza L, van der Schans G P, Lohman P H
Mutat Res. 1985 Jul;146(1):89-98. doi: 10.1016/0167-8817(85)90059-8.
Irradiation with UV-A of normal human fibroblasts in phosphate-buffered saline induced cell death, measured as lack of colony-forming ability. A specially filtered sunlamp, emitting wavelengths greater than 330 nm, was used as UV-A source. After UV-A irradiation, single-strand breaks (alkali-labile bonds) could be detected in DNA; these lesions were rapidly repaired. The induction of these single-strand breaks was almost eliminated when irradiation was performed in the presence of catalase. However, catalase, when present during UV-A irradiation, did not reduce cell death of the fibroblasts. Excision repair, monitored as unscheduled DNA synthesis, was induced strongly by irradiation with UV-C (predominantly 254 nm), but could not be detected after UV-A irradiation. Moreover, very little accumulation of incision breaks during post-irradiation incubation with hydroxyurea and 1-beta-D-arabinofuranosylcytosine (araC) was detected after UV-A. This is consistent with the low amount of pyrimidine dimers (measured as UV-endonuclease susceptible sites) induced by UV-A. Xeroderma pigmentosum fibroblasts of complementation group A, which are extremely sensitive to UV-C irradiation, showed the same sensitivity to UV-A as normal fibroblasts. The results indicate that lethality by UV-A wavelengths greater than 330 nm is caused by lesions other than single-strand breaks (alkali-labile bonds) and pyrimidine dimers.
在磷酸盐缓冲盐溶液中，用紫外线A（UV-A）照射正常人成纤维细胞会导致细胞死亡，通过缺乏集落形成能力来衡量。使用一种经过特殊滤光的太阳灯作为UV-A源，该太阳灯发射波长大于330nm的光。UV-A照射后，可在DNA中检测到单链断裂（碱不稳定键）；这些损伤会迅速修复。当在过氧化氢酶存在的情况下进行照射时，这些单链断裂的诱导几乎被消除。然而，在UV-A照射期间存在过氧化氢酶时，并不会降低成纤维细胞的细胞死亡。以非预定DNA合成来监测的切除修复，在紫外线C（主要为254nm）照射后被强烈诱导，但在UV-A照射后无法检测到。此外，在UV-A照射后，在用羟基脲和1-β-D-阿拉伯呋喃糖基胞嘧啶（araC）进行照射后孵育期间，几乎检测不到切口断裂的积累。这与UV-A诱导的嘧啶二聚体数量较少（以对紫外线内切酶敏感的位点来衡量）是一致的。A互补组的着色性干皮病成纤维细胞对紫外线C照射极为敏感，对UV-A的敏感性与正常成纤维细胞相同。结果表明，波长大于330nm的UV-A导致的致死性是由单链断裂（碱不稳定键）和嘧啶二聚体以外的损伤引起的。
