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The True Cause of Sunburn: Beyond Just Genetics


You might be surprised to discover what actually triggers those immediate sunburn reactions, such as inflammation and cell death.

For many years, scientists attributed the painful red sunburn that follows excessive sun exposure to DNA damage. However, recent findings suggest they may have been looking in the wrong direction.

A study published in December 2024 uncovered that RNA damage is the real instigator behind the immediate painful effects of sunburn, challenging our previous understanding of how ultraviolet (UV) radiation impacts the skin.

The research, featured in Molecular Cell, revealed that while UV radiation harms both RNA and DNA, it is the damage to RNA that initiates sunburn’s immediate skin reactions, such as inflammation and cell death. 

Interestingly, the study did not explore the broader implications of RNA being the culprit behind sunburn reactions.

“Traditionally, it has been stated that sunburn damages the DNA, resulting in cell death and inflammation. But this study enlightened us that the acute effects of sunburn stem from RNA damage, not DNA,” stated Anna Constance Vind, assistant professor at the Department of Cellular and Molecular Medicine at the University of Copenhagen and one of the researchers behind the study, in a press release.

Unlike DNA, which contains permanent genetic information susceptible to lasting changes affecting new cells, RNA is a short-lived molecule engaged in specific tasks, making its damage a temporary issue.

“Although RNA has a shorter lifespan than DNA, it doesn’t mean that RNA damage is unimportant or trivial,” remarked Dr. Hannah Kopelman, a dermatologist specializing in aesthetic surgery and skin cancer at Boston University, who was not part of the study. “RNA is vital for protein production; if it gets damaged, it can result in errors in protein synthesis or even halt the creation of essential proteins. This can disrupt cellular functions, despite RNA’s transient nature.”

She elaborated that such disruptions could impair significant skin functions, like preserving the skin barrier.

“Over time, these disturbances can weaken the skin’s resilience and hasten visible aging signs such as fine lines, wrinkles, and loss of elasticity,” she emphasized.

When the Sun Burns the Skin

In contrast to earlier beliefs attributing sunburns to DNA damage, this new study indicates that RNA damage—not DNA—elicits the skin’s early stress response.

Our bodies have internal defense mechanisms that react to cellular damage caused by stressors like UV radiation, with ZAK-alpha, a protein activated during cell damage, playing a critical role.

Recent research has identified ZAK-alpha as the primary responder to RNA damage induced by UV radiation, triggering a cellular emergency signal that results in inflammation and cell death.

To examine ZAK-alpha’s role, researchers from the University of Copenhagen and Nanyang Technological University, Singapore, exposed both mouse and human skin cells along with living mice—to UV radiation with and without the presence of ZAK-alpha, comparing their reactions.

They discovered that ZAK-alpha identifies RNA damage and provokes early skin inflammation and cell death within hours following UV exposure.

Indicators of ZAK-alpha activation include the typical sunburn symptom of thickened skin, often characterized by a leathery texture. Other symptoms including pain, itching, blistering, and wound formation shortly after sun exposure also result from ZAK-alpha activation.

Mice expressing the ZAK-alpha protein experienced more than threefold skin thickening within 24–48 hours compared to those lacking it.

UV Rays Damage RNA and DNA

The study determined that a single dose of UV exposure resulted in damage to both RNA and DNA. While RNA damage manifested immediately, DNA damage became apparent after a period of 24 hours.

UV radiation inflicts damage on DNA by creating breaks and abnormal linkages among DNA bases, leading to distortions that induce errors during DNA replication, which can have grave consequences for the cell, including cell death and a heightened cancer risk.

“Long-term and excessive UV exposure leads to the accumulation of such damage, increasing the probability of mutations in key genes responsible for suppressing tumors,” stated Kopelman, indicating that the buildup of these mutations can contribute to the onset of skin cancers like melanoma.

Moreover, studies indicate that RNA damage, irrespective of its source, could indirectly result in DNA damage by disrupting crucial cellular functions or instigating responses that may lead to DNA instability or damage.

“When RNA is impaired, the cell’s normal machinery is thrown off course, which can lead to both immediate and cumulative consequences,” Kopelman explained.

Rethinking Sunburn Treatments

Most treatments for sunburn primarily focus on alleviating symptoms like pain and swelling rather than fixing DNA damage. Nevertheless, prior assumptions linking sunburn reactions to DNA damage have led to the inclusion of DNA repair ingredients in some skincare products.

The World Health Organization recommends avoiding excessive sun exposure, especially in the two hours before and after noon, due to the increased likelihood of skin cancer resulting from DNA damage. They advocate seeking shade, donning protective clothing, and applying broad-spectrum sunscreen to block harmful UV rays.

The body initiates repair of DNA damage due to UV sun exposure as soon as it occurs. Nonetheless, these repair mechanisms are not foolproof. Incomplete or ineffective DNA repair can lead to mutations, elevating the risk of skin cancer and other ailments.

“Certain skincare products incorporate DNA repair enzymes, like photolyase sourced from plankton extract, which can identify and mend UV-induced DNA lesions. When applied topically, these enzymes aim to rectify damage at the molecular level, potentially decreasing the risk of skin cancers and alleviating signs of photoaging,” remarked Kopelman.

Using these enzymes in skin care may aid in repairing UV-induced DNA damage and specifically reduce a type of DNA damage known as cyclobutane pyrimidine dimers, a leading cause of skin cancer, she explained.

As our knowledge of UV-induced damage and repair approaches continues to progress, Kopelman posits that integrating preventive strategies with innovative treatments targeting both DNA and RNA repair presents a holistic method for managing and mitigating the harmful effects of UV exposure.



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