How UVA Damages Mitochondrial DNA – And How Antioxidants Can Help
A new study conducted by ETH Zurich and the University Hospital Zurich, with support from Mibelle Biochemistry and the Mibelle Group, reveals fresh insights into how UVA light accelerates mitochondrial aging in the skin.
Mitochondria & the “Common Deletion”
UVA penetrates deeply into the dermis, where it increases the production of reactive oxygen species (ROS). This leads to oxidative damage in mitochondrial DNA (mtDNA). One specific type of damage, the Common Deletion (a large 4977 base pair loss), accumulates in sun‑exposed skin and serves as a potential biomarker of mitochondrial stress and photoaging.
What the Study Found
- UVA strongly increases ROS, leading to oxidative mtDNA damage.
- This oxidative stress promotes the formation of the Common Deletion in mitochondria of both fibroblasts and keratinocytes.
- UVB acts differently, causing direct DNA photoproducts rather than ROS.
- RNA-Seq analysis of the transcriptome of fibroblasts revealed changes in mitochondrial gene expression upon UVA exposure, extending the effect beyond mtDNA damage
- The effects were confirmed in a 3D full-thickness skin model, demonstrating high physiological relevance.
Antioxidants Offer Protection
The study shows that antioxidants can significantly reduce UVA‑induced mtDNA damage and lower the Common Deletion level. This highlights antioxidants as effective strategies to support mitochondrial integrity, even under strong UVA stress.
Relevance for Cosmetic Innovation
- Mitochondrial health is a central factor in photoaging.
- The Common Deletion can serve as a quantifiable biomarker for testing antioxidant or UVA-protective actives.
- Antioxidants demonstrate protective effects at the mitochondrial level and are thus highly relevant for modern anti-aging formulations.
The newly established 3D full‑thickness skin model can now be applied in further studies to systematically evaluate active compounds and plant extracts for their ability to prevent mitochondrial damage and, consequently, prevent skin aging processes.
Acknowledgements
We extend our sincere thanks to the research teams at ETH Zurich and University Hospital Zurich for their outstanding scientific work.
Find the Publication here.
Special appreciation goes to the study’s authors: Gabriele A. Fontana, Navnit K. Singh, Nadezhda Rotankova, Antonia Eichelberg, Michela Di Filippo, Michael R. MacArthur, Susanne Heldmaier, Franziska Wandrey, Hans Dietmar Beer, Shana J. Sturla, and Hailey L. Gahlon.
