Cleaver J E
Mech Ageing Dev. 1984 Oct 15;27(2):189-96. doi: 10.1016/0047-6374(84)90044-7.
Senescence of skin fibroblast cultures from normal individuals occurred after 23.9 +/- 6.3 (S.D.) passages; senescence in DNA repair-deficient cell lines from xeroderma pigmentosum patients occurred at 22.9 +/- 5.5 passages. Cells from xeroderma pigmentosum variant and Cockayne syndrome patients reached senescence at similar passage numbers. Xeroderma pigmentosum patients contract skin cancer as a consequence of their repair deficiencies but show no symptoms of premature ageing; neither do their cells age prematurely in vitro. The clinical spectrum and the life-span of fibroblasts in culture therefore lend no support for a correlation between ageing and the DNA repair or DNA replication deficiencies found in xeroderma pigmentosum and Cockayne syndrome cells.
来自正常个体的皮肤成纤维细胞培养物在传代23.9±6.3（标准差）次后出现衰老；来自着色性干皮病患者的DNA修复缺陷细胞系在传代22.9±5.5次时出现衰老。着色性干皮病变异型和科凯恩综合征患者的细胞在相似的传代次数时达到衰老。着色性干皮病患者由于其修复缺陷而患皮肤癌，但没有早衰症状；他们的细胞在体外也不会过早衰老。因此，培养的成纤维细胞的临床谱和寿命不支持衰老与在着色性干皮病和科凯恩综合征细胞中发现的DNA修复或DNA复制缺陷之间存在关联。
