Affiliation:
1. Consumer and Clinical Radiation Protection Bureau Health Canada Ottawa Ontario Canada
2. Environmental Health Science and Research Bureau Health Canada Ottawa Ontario Canada
3. Department of Biology University of Ottawa Ottawa Ontario Canada
Abstract
AbstractExposure to ultraviolet radiation (UV‐R), from both natural and artificial tanning, heightens the risk of skin cancer by inducing molecular changes in cells and tissues. Despite established transcriptional alterations at a molecular level due to UV‐R exposure, uncertainties persist regarding UV radiation characterization and subsequent genomic changes. Our study aimed to mechanistically explore dose‐ and time‐dependent gene expression changes, that may drive short‐term (e.g., sunburn) and long‐term actinic (e.g., skin cancer) consequences. Using C57BL/6N mouse skin, we analyzed transcriptomic expression following exposure to five erythemally weighted UV‐R doses (0, 5, 10, 20, and 40 mJ/cm2) emitted by a UV‐R tanning device. At 96 h post‐exposure, 5 mJ/cm2 induced 116 statistically significant differentially expressed genes (DEGs) associated with structural changes from UV‐R damage. The highest number of significant gene expression changes occurred at 6 and 48 h post‐exposure in the 20 and 40 mJ/cm2 dose groups. Notably, at 40 mJ/cm2, 13 DEGs related to skin barrier homeostasis were consistently perturbed across all timepoints. UV‐R exposure activated pathways involving oxidative stress, P53 signaling, inflammation, biotransformation, skin barrier maintenance, and innate immunity. This in vivo study's transcriptional data offers mechanistic insights into both short‐term and potential non‐threshold‐dependent long‐term health effects of UV‐R tanning.