Photoprotection from UV light-induced telomere shortening and DNA damage by a broad-spectrum sunscreen.

BACKGROUND

Ultraviolet (UV) radiation contributes to photoaging and skin cancer by causing DNA damage and generating reactive oxygen species (ROS). It also induces telomere shortening, a key factor in cellular aging. However, no studies have investigated whether sunscreen can prevent short-term telomere shortening caused by UV exposure to human skin.

OBJECTIVES

We have examined whether the use of a broad-spectrum sunscreen product can protect at the telomere level from the harmful effects of UV light.

METHODS

Human keratinocytes and a 3D skin model were exposed to 10 J/cm2 of solar-simulated UV radiation under three conditions: non-exposed, exposed, and exposed with broad-spectrum sunscreen. DNA damage, assessed by γH2AX levels, was measured at 30 min and 24 h post-irradiation. Telomere length was evaluated by high-throughput quantitative fluorescence in situ hybridization (HT Q-FISH) at 24 h post-irradiation. Histological analysis of 3D skin samples was performed using hematoxylin and eosin (H&E) staining to assess tissue integrity.

RESULTS

A decrease in cell number, increased DNA damage, and telomere shortening, accompanied by a higher proportion of critically short telomeres, were observed in UV-exposed keratinocytes and reconstructed human skin following exposure to 10 J/cm2 of solar-simulated UV radiation. The 3D skin architecture was also compromised, showing loss of keratinocytes spatial organization, evidence of epidermal cell death, and significant dermal thinning. However, cells and 3D skin samples protected with a broad-spectrum sunscreen remained comparable to non-exposed controls, showing no detectable structural or molecular alterations.

CONCLUSIONS

These findings provide initial evidence that a broad-spectrum sunscreen product can mitigate UV-induced telomere shortening and DNA double-strand damage (DSBs), thereby preventing photodamage associated with solar exposure.