The skin, as the body’s largest organ, is constantly exposed to environmental stressors, with sunlight being one of the most extensively studied. Sunlight comprises ultraviolet radiation (UVR), visible light, and infrared radiation (IR), each contributing to various effects on skin health. While the deleterious effects of UVR—such as photoaging and skin cancer—are well-established, the impact of visible light, particularly blue light (400–500 nm), is increasingly recognized as a significant concern for skin aging. Blue light exposure, from both the sun and electronic devices, is associated with issues like hyperpigmentation, altered skin cell morphology, collagen degradation, and decreased cell viability and proliferation.
Given these cumulative threats, sun protection products remain a primary strategy to mitigate sunlight’s adverse effects. Sunscreens have proven effective in reducing photoaging and skin cancer risks. However, there is a growing need to evaluate how well these products defend against blue light and the deeper cellular mechanisms involved. Mitochondrial DNA (mtDNA), located close to the source of reactive oxygen species (ROS), lacks protective histones and has limited repair mechanisms—making it a highly sensitive biomarker for UV-induced damage. This study investigated how commercial sun protection products perform in shielding human dermal fibroblast skin cells from UV-induced mtDNA damage and blue light-induced cell decline.
Methods
The study evaluated the efficacy of four SPF 50 commercial sun protection products—both mineral and organic/chemical formulations—on their ability to prevent UV-induced mtDNA damage and blue light-related cell viability loss. Products were applied at 2 mg/cm² to PMMA plates layered with tape and placed between light sources and cultured human dermal fibroblast cells. Cells were exposed to 2 standard erythemal doses of UVR or 50 J/cm² of blue light. Mitochondrial DNA damage was measured via real-time qPCR, and cell viability post-blue light exposure was evaluated using MTS assays.
Key Findings
- All four SPF 50 products significantly reduced UV-induced mtDNA damage in skin cells compared to unprotected exposure.
- UV-exposed cells without sunscreen exhibited greater mtDNA damage, validating the test setup and reinforcing sunscreen efficacy.
- Two SPF 50 products (one chemical-based and one mineral-based) successfully protected against blue light-induced drops in cell viability.
- The mineral-based sunscreen outperformed the chemical one in protecting cells from blue light.
- Cell viability was lowest in the absence of any sun protection, underscoring the importance of product application.
This study presents direct evidence that SPF 50 sunscreens offer meaningful protection not only from UV-induced mitochondrial DNA damage but also from blue light-related cellular decline. By maintaining mitochondrial integrity, sunscreens help preserve cellular energy and reduce signs of fatigue and premature aging. The superior performance of mineral-based products against blue light damage also hints at opportunities for future innovation in formulation design.
These results encourage the daily, consistent use of broad-spectrum SPF products—not just for UV defense, but for comprehensive skin protection in our increasingly digital and sun-exposed environments. As awareness of blue light grows, so too should attention to product ingredients that guard against its impact. This research lays the foundation for next-generation sunscreen development that fully addresses modern environmental stressors.
Link to the study: https://www.mdpi.com/2079-9284/12/3/128
