Prolonged DNA damage at suberythemal UV dose – Dependency on skin type and age

Ultraviolet radiation (UVR) is the primary risk factor for skin cancer, inducing DNA damage such as cyclobutane pyrimidine dimers (CPD) and pyrimidine–pyrimidone (6–4) photoproducts. DNA repair is influenced by age and skin type. Aging reduces repair capacity, leading to accumulated DNA damage, while darker skin provides some protection through melanin's UV-absorbing properties. However, repair dynamics in darker skin remain poorly understood.

This pilot study aimed at evaluating the influence of age and skin pigmentation on UV-induced DNA damage and repair efficiency in both ex vivo skin samples and healthy volunteers. Excised skin samples were categorized by pigmentation and age: light skin (types I–II, 18–50 years), light skin (55–70 years), and dark skin (types IV–V, 18–50 years). Samples were irradiated with fixed suberythemal doses, and biopsies were collected immediately post-irradiation to evaluate DNA damage and p53 expression. Healthy volunteers, grouped similarly (n = 6 per group), received ¼ minimal erythema dose (MED, determined individually), with biopsies taken 24 h and 7 days after irradiation. For melanin dependence, DNA damage was also determined directly after irradiation.

Older individuals exhibited greater DNA damage and reduced repair capacity. Dark skin showed initial melanin-mediated protection; but a first hint of greater residual damage was observed 24 h after irradiation compared to light skin, probably due to delayed repair activation and melanin photosensitization. However, the high variability in dark skin underscores the need for larger, diverse studies to better understand pigmentation-related differences in UV response and DNA repair mechanisms. By day seven, CPD clearance was observed in dark skin.

These findings highlight that even suberythemal UVR induces photodamage, with repair kinetics influenced by age and pigmentation.