Wang S M, Nishigori C, Yagi T, Takebe H
Department of Experimental Radiology, Faculty of Medicine, Kyoto University, Japan.
Mutat Res. 1991 Jan;256(1):59-66. doi: 10.1016/0921-8734(91)90034-9.
A reduction in the amount of UV-induced unscheduled DNA synthesis (UDS), and reduced cell survival and host-cell reactivation against UV exposure in Hutchinson-Gilford progeria syndrome cell strains were shown. UV-induced UDS in 4 progeria cell strains was 33-50% of the normal level. A similar reduction in the UV-induced UDS in normal cells was caused by gamma-ray irradiation to the cells before UV irradiation. The dose of gamma-rays required to cause a reduction in UDS of normal cells to the level of progeria cells was 40 Gy and the reduction was reversible after 2 days. In progeria cells, gamma-ray irradiation further reduced UDS with a lower gamma-ray dose required than in normal cells, and the reduction was also reversible but with less relative recovery than in normal cells. The presence of a 'built-in' defect in progeria cells responsible for the reduced DNA-repair capacity was suggested, and such defect may share a common mechanism with the reduction of UV-induced UDS in normal cells caused by gamma-ray irradiation.
研究表明，在哈钦森-吉尔福德早衰综合征细胞株中，紫外线诱导的非定规DNA合成（UDS）量减少，细胞存活率降低，且对紫外线照射的宿主细胞复活能力下降。4种早衰细胞株中紫外线诱导的UDS为正常水平的33%-50%。在紫外线照射前对正常细胞进行γ射线照射，可导致正常细胞中紫外线诱导的UDS出现类似程度的降低。使正常细胞UDS降低至早衰细胞水平所需的γ射线剂量为40 Gy，且2天后这种降低是可逆的。在早衰细胞中，γ射线照射以比正常细胞更低的γ射线剂量进一步降低了UDS，这种降低也是可逆的，但相对恢复程度低于正常细胞。这表明早衰细胞中存在一种导致DNA修复能力降低的“内在”缺陷，且这种缺陷可能与γ射线照射导致正常细胞中紫外线诱导的UDS降低具有共同机制。
