For years, we’ve been warned about the dangers of too much sun exposure, mainly between noon and 3 p.m. The standard advice is to avoid direct sunlight, seek shade, and wear sunscreen and a hat. Despite these precautions, many people have experienced the discomfort of sunburn, where the skin turns bright red, becomes irritated, and requires cooling relief.
We’ve all been told sunburn damages DNA, but new research suggests this widely accepted explanation may not be entirely accurate.
A groundbreaking study led by researchers from the University of Copenhagen and Nanyang Technological University (NTU) in Singapore has uncovered a surprising new finding: it’s not the DNA, but rather RNA, that plays a crucial role in triggering the harmful effects of sunburn.
“Sunburn damages the DNA, leading to cell death and inflammation. So the textbooks say. But in this study, we were surprised to learn that it damages the RNA that causes the acute effects of sunburn,” explains Assistant Professor Anna Constance Vind from the University of Copenhagen’s Department of Cellular and Molecular Medicine.
The study challenges conventional wisdom about the mechanics of sunburn. While DNA is known to store genetic information and can be passed down through generations, RNA is a more transient molecule that plays a crucial role in translating genetic information into the proteins that make up our cells.
Super melanin: Skin savior for sunburn and chemical burns
RNA, particularly messenger RNA (mRNA), has long been considered less critical than DNA. Previously, scientists assumed that RNA damage was less consequential as long as DNA remained intact. However, the new study reveals that RNA damage is the first response to UV radiation, triggering cellular events that lead to inflammation and cell death.
The researchers discovered that UV radiation damages RNA, creating a complex response within the cells. This response is regulated by a protein called ZAK-alpha, which acts as a “surveillance system” to monitor RNA integrity. When damage occurs, ZAK-alpha triggers inflammation and immune responses, leading to the familiar symptoms of sunburn, such as redness, pain, and swelling.
“We found that the cells’ initial response to UV exposure is not DNA damage, as previously thought, but RNA damage,” says Professor Simon Bekker-Jensen, another lead researcher from the University of Copenhagen. “This triggers cell death and inflammation. In experiments with mice, when we removed the ZAK gene, these responses were significantly reduced, suggesting that ZAK plays a key role in the skin’s defense against UV damage.”
The study also highlights how this RNA-based response is quicker and more efficient than DNA-based damage repair. The research suggests that RNA damage activates a more immediate defense mechanism, helping the skin to respond rapidly and effectively to prevent further harm.
“This is a paradigm shift in our understanding of sunburn,” says Vind. “We used to think that DNA damage controlled the skin’s initial response to UV radiation, but now we know that RNA damage triggers a faster and more effective response.”
The study has important implications for understanding and treating sunburn and other skin-related conditions.
Dr. Franklin Zhong, co-author of the study and Nanyang Assistant Professor at NTU’s Lee Kong Chian School of Medicine, points out that many chronic inflammatory skin diseases are aggravated by sun exposure. By understanding how RNA damage drives the body’s response to UV radiation, new treatments for these conditions could emerge.
“We may need to rethink our approach to preventing and treating sunburn, particularly in people with chronic skin conditions,” says Dr. Zhong. “This new knowledge could open the door to innovative therapies.”
The research overturns decades of established understanding about the biological effects of UV radiation, and experts agree that textbooks will need to be updated to reflect this new insight.
“It’s a game changer,” says Professor Bekker-Jensen. “For years, we’ve associated sunburn with DNA damage. Now, we need to rewrite the textbooks. This discovery will shape future research on UV radiation’s effects on the skin.”
As our understanding of sunburn continues to evolve, it’s clear that protecting our skin from UV radiation is more critical than ever—and that the story of how our bodies react to the sun may be far more complex than we once thought.
Journal Reference:
- Anna Constance Vind, Zhenzhen Wu, Muhammad Jasrie Firdaus et al. The ribotoxic stress response drives acute inflammation, cell death, and epidermal thickening in UV-irradiated skin in vivo. Molecular Cell. DOI: 10.1016/j.molcel.2024.10.044
Source: Tech Explorist