For decades, scientists blamed DNA damage for the angry red sunburn that follows a day of too much sun. But they may have been pointing fingers at the wrong molecular culprit.
A December 2024 study identified RNA damage as the true instigator of sunburn’s immediate painful effects, upending our understanding of how ultraviolet (UV) radiation affects our skin.
The study, published in Molecular Cell, found that UV radiation damages both RNA and DNA, but it’s RNA damage that triggers sunburn’s initial skin reactions like inflammation and cell death.
However, the study did not mention any other implications of learning that RNA, and not DNA, is the culprit behind 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 this is a result of damage to the RNA, not the DNA that causes the acute effects of sunburn,” Anna Constance Vind, assistant professor at the Department of Cellular and Molecular Medicine at the University of Copenhagen, and one of the researchers responsible for the new study, said in a press release.
Because DNA stores permanent genetic information, its damage can lead to lasting changes passed on to new cells, unlike RNA, a short-lived molecule used for specific tasks, whose damage is temporary.
“While it’s true that RNA is more short-lived than DNA, RNA damage isn’t necessarily ‘better’ or less significant,” Dr. Hannah Kopelman, a dermatologist at Aesthetic Surgery and skin cancer dermatology fellow at Boston University, who was not involved in the study, told The Epoch Times.
“RNA plays a key role in protein production, so if it’s damaged, it can lead to errors in making proteins or even stop essential proteins from being made. This can disrupt how cells function, even though RNA doesn’t last as long as DNA.”
She further explained that this disruption can impair key skin functions, such as maintaining the skin barrier.
“Over time, these disruptions can weaken the skin’s resilience and accelerate visible signs of aging, like fine lines, wrinkles, and loss of elasticity,” she noted.
When the Sun Burns the Skin
Contrary to previous beliefs that sunburns were caused by DNA damage, the new study found that RNA damage—not DNA—triggers the skin’s early stress response.
Our bodies have internal defense systems that respond to cell damage from stressors like UV rays and ZAK-alpha, a protein that gets activated during cell damage.
Recent studies have found that ZAK-alpha is the main sensor of RNA damage from UV radiation, triggering a cellular emergency alarm that leads to inflammation and cell death.
To better understand ZAK-alpha’s role, researchers from the University of Copenhagen and Nanyang Technological University, Singapore, exposed mouse and human skin cells and live mice—with and without the ZAK-alpha—to UV radiation and compared their responses.
They found that ZAK-alpha detects RNA damage and triggers early skin inflammation and cell death within a couple of hours of UV exposure.
Symptoms of ZAK-alpha activation include the stereotypical sunburn symptom of thickened skin, often described as leathery texture. Other symptoms like pain, itching, blistering, and wounding soon after sun exposure are also caused by ZAK-alpha activation.
Mice with the ZAK-alpha protein showed more than three times the skin thickening within 24–48 hours compared to mice without it.
UV Rays Damage RNA and DNA
Based on the study, a single UV exposure dose led to RNA and DNA damage. While RNA damage was the immediate response, DNA damage became evident after 24 hours.
UV radiation damages DNA by causing breaks and abnormal linkages between DNA bases, which are the building blocks of DNA. These distortions lead to errors during DNA replication, resulting in mutations that can have serious consequences for the cell, including cell death and an increased risk of cancer.
“Chronic and excessive UV exposure increases the accumulation of such damage, elevating the risk of mutations in critical genes that suppress tumors,” Kopelman said, adding that accumulation of these tumors can initiate the development of skin cancers like melanoma.
However, studies show that RNA damage, regardless of the source, may indirectly cause DNA damage by disrupting essential cellular processes or triggering cellular responses that could lead to DNA instability or damage.
“Essentially, when RNA is damaged, the cell’s normal ’machinery' gets thrown off balance, which can have both immediate and cumulative effects,” Kopelman said.
Reevaluating Sunburn Treatments
Most sunburn treatments focus on soothing symptoms like pain and swelling rather than repairing DNA damage. However, previous assumptions of sunburn reactions being linked to DNA damage have led to some skin care products containing ingredients for DNA repair.
The World Health Organization advises against excessive sun exposure, particularly two hours before and after noon, due to the increased risk of skin cancer caused by DNA damage. They recommend seeking shade, wearing protective clothing, and using broad-spectrum sunscreens to block harmful UV rays.
The body repairs DNA damage caused by UV sun exposure as soon as it is formed. However, these repair systems are not foolproof. Incomplete or faulty DNA repair can lead to mutations, increasing the risk of skin cancer and other diseases.
“Certain skin care products contain DNA repair enzymes, such as photolyase derived from plankton extract, which can recognize and repair UV-induced DNA lesions. When applied topically, these enzymes work to correct damage at the molecular level, potentially reducing the risk of skin cancers and mitigating signs of photoaging,” said Kopelman.
Using these enzymes in skin care can help repair UV-induced DNA damage and reduce a particular type of DNA damage called cyclobutane pyrimidine dimers, which are a major cause of skin cancer, she said.
While our understanding of UV-induced damage and repair mechanisms continues to evolve, Kopelman believes that combining preventive measures with innovative treatments targeting DNA and RNA repair offers a comprehensive approach to managing and mitigating the harmful effects of UV exposure.