DNA repair in cultured human fibroblasts does not decline with donor age

Human fibroblasts from young (3 days to 3 years) and old (84–94 years) donors were tested for their ability to repair DNA damage by measuring survival of colony formation following irradiation with ultraviolet (UV) light. Repair was also measured by the ability to reactivate herpes simplex virus following treatment of the virus with UV light, methyl methane sulfonate or 4,5′,8-trimethylpsoralen plus light. This virus was used as a probe of cellular repair capacity because survival of damaged virus is lower in repair-deficient cell lines [1]. Cell lines from both age groups exhibited comparable survivals following UV irradiation and failed to show increased sensitivity to irradiation in the presence of caffeine. Cells from both groups repaired damaged virus to equal extents. Proficient viral repair was observed under conditions in which cells were infected by either single or multiple viral genomes. These results suggest that DNA repair mechanisms which act on a variety of lesions (e.g. pyrimidine dimers, apurinic sites, alkylated bases, cross-links, etc.) do not decline with age. A model for biological aging resulting from the accumulation with age of unrepaired DNA damage is discussed.