Too much sun results in RNA damage to your skin cells
We are reminded time and time again of how much sunburn hurts. But what exactly happens during this reddish and painful experience?
Researchers at the University of California's San Diego School of Medicine have found, using both human skin cells and mouse models, that the biological mechanism of sunburn - an immune response to ultraviolet radiation - is the result of RNA damage to skin cells.
Reporting their findings in Nature Medicine, the scientists say it could open the way to eventually blocking the inflammatory process, and have implications for a range of medical conditions and treatments.
RNA, or ribonucleic acid, is a type of molecule very similar to DNA, the hereditary material in humans and almost all other living organisms. RNA plays an active role in cell processes such as biological reactions and protein synthesis.
Principal investigator Dr Richard L. Gallo and his team found that UVB radiation - the part of the electromagnetic spectrum that causes sunburn - fractures and tangles elements of a special type of RNA inside the cell that does not directly make proteins. Irradiated cells release the altered RNA, causing healthy, neighbouring cells to start a process that results in an inflammatory response intended to remove the sun-damaged cells. This process is what we see and feel as sunburn.
'The inflammatory response is important to start the process of healing after cell death,' says Gallo, professor of medicine and paediatrics at UC San Diego School of Medicine.
'We also believe that the inflammatory process may clean up cells with genetic damage before they can become cancerous.
'Of course, this process is imperfect and with more UV exposure, there is more chance of cells becoming cancerous.'
With this discovery, the scientists hope to explore how to help patients with conditions related to UV light exposure.
'For example, diseases such as psoriasis are treated by UV light, but a big side effect is that this treatment increases the risk of skin cancer,' says Gallo. 'Our discovery suggests a way to get the beneficial effects of UV therapy without actually exposing our patients to the harmful UV light. Also, some people have excess sensitivity to UV light, patients with lupus, for example. We are exploring if we can help them by blocking the pathway we discovered.'
Meanwhile, Gallo says it's still not known how gender, skin pigmentation and individual genetics may affect the mechanism of sunburn. 'Genetics is closely linked to the ability to defend against UV damage and develop skin cancers,' he says.
'We know in our mouse genetic models that specific genes will change how the mice get sunburn.
'Humans have similar genes, but it is not known if people have mutations in these genes that affect their sun response.'