Tsongalis G J, Lambert W C, Lambert M W
Department of Pathology, UMDNJ-New Jersey Medical School, Newark 07103.
Mutat Res. 1990 Jul;244(3):257-63. doi: 10.1016/0165-7992(90)90138-a.
Cells from patients with xeroderma pigmentosum, complementation group A (XPA), are known to be defective in repair of pyrimidine dimers and other forms of damage produced by 254-nm ultraviolet (UVC) radiation. We have isolated a DNA endonuclease, pI 7.6, from the chromatin of normal human lymphoblastoid cells which recognizes damage produced by UVC light, and have introduced this endonuclease into UVC-irradiated XPA cells in culture to determine whether it can restore their markedly deficient DNA repair-related unscheduled DNA synthesis (UDS). Introduction of the normal endonuclease, which recognizes predominantly pyrimidine dimers, but not the corresponding XPA endonuclease into UVC-irradiated XPA cells restored their levels of UDS to approximately 80% of normal values. Electroporation of both the normal and the XPA endonuclease into normal human cells increases UDS in normal cells to higher than normal values. These results indicate that the normal endonuclease can restore UDS in UVC-irradiated XPA cells. They also indicate that XPA cells have an endonuclease capable of increasing the efficiency of repair of UVC damage in normal cells.
患有A型着色性干皮病（XPA）的患者的细胞，已知在嘧啶二聚体及254纳米紫外线（UVC）辐射产生的其他形式损伤的修复方面存在缺陷。我们从正常人淋巴母细胞的染色质中分离出一种DNA内切酶，其pH值为7.6，该酶能识别UVC光产生的损伤，并将这种内切酶引入培养的经UVC照射的XPA细胞中，以确定它是否能恢复其明显缺乏的与DNA修复相关的非定
期DNA合成（UDS）。将主要识别嘧啶二聚体的正常内切酶而非相应的XPA内切酶引入经UVC照射的XPA细胞，可使其UDS水平恢复到正常值的约80%。将正常和XPA内切酶电穿孔导入正常人细胞，会使正常细胞中的UDS增加到高于正常值的水平。这些结果表明，正常内切酶可恢复经UVC照射的XPA细胞中的UDS。它们还表明，XPA细胞有一种内切酶，能够提高正常细胞中UVC损伤的修复效率。
