Feeling the Heat: the Science of Sunburn


No matter how careful we are, at some point in all of our lives we will develop sunburn.  Despite all of the NHS campaigns and warnings that sun damage can cause skin cancer, many of us will know at least one person who forgoes using suncream and lets themselves bake in the sun in the quest for the perfect summer glow.  But what is sunburn?  And why is it so dangerous?  First we need to take a look at our skin.

All of us have a pigment called Melanin in our skin- some of you will already know it as the protein that determines skin colour.  But Melanin also acts to absorb UV light, releasing it as heat, protecting our cells from these damaging rays.  When radiation gets through this barrier and starts to damage our cells, the body senses this and floods the area with blood, also inducing inflammation that causes those damaged cells to be shed, helping to stop the accumulation of damage that can lead to the formation of cancers.

Noncoding RNA (RNA molecules that don’t code for proteins) have been shown to play a part in the recognition of this damage to our cells.   It has been shown that these RNA are released from keratinocytes after UV radiation, stimulating the release of the inflammatory cytokines TNF-alpha and IL-6, which can also induce apoptosis in cells.  UVB radiation was shown to alter double stranded regions of certain noncoding RNAs such as U1, and this change was enough to induce cytokine production as well as inducing production of NF-kB.  This UV response was mediated by the RNA binding to Toll-like receptor 3 (TLR3).

If you’ve ever read the back of a bottle of sunscreen you’ll already know that UV radiation exists in a number of different forms, the most damaging and carcinogenic being UVB rays.  UVB is responsible for the formation of DNA lesions, most notably pyrimidine dimers and pyrimidine-pyrimidone photoproducts. Both of these historically would have been repaired by proteins called photolyases which recognise the damage through the distortion of the DNA helix by the lesions. However, placental mammals (like us!) have lost this capability over time and now must use other repair pathways (such as nucleotide excision repair) to fix the lesions.  There is a huge amount of interplay between our DNA repair pathways and the proteins involved in this, and it’s really important that the DNA that codes for these proteins aren’t themselves damaged by UV and other damaging agents or these mechanisms can fail.

With Cancer Research UK stating that around 86% of of malignant melanomas are linked to our lifestyle, it’s really important that we take care of our skin!


If you enjoyed this article, you may also like:

The Hallmarks of Cancer

DNA repair, why should you care?

Biological Pacemakers, A Hearty Improvement?


Bernard JJ, Cowing-Zitron C, Nakatsuji T, Muehleisen B, Muto J, Borkowski AW, Martinez L, Greidinger EL, Yu BD, & Gallo RL (2012). Ultraviolet radiation damages self noncoding RNA and is detected by TLR3. Nature medicine, 18 (8), 1286-90 PMID: 22772463

Lima-Bessa, K., & Menck, C. (2005). Skin Cancer: Lights on Genome Lesions Current Biology, 15 (2) DOI: 10.1016/j.cub.2004.12.056

Image from- https://www.flickr.com/photos/esther-/1791843722/


3 responses to “Feeling the Heat: the Science of Sunburn

  1. I know this is a silly question, but I’m curious, and in the case that you can answer my question, here it goes. How did proteins called photolyases repair lesions in placental mammals before they “evolved”? Surge the body? What exactly.
    _From one who notices the little details_

    • Hi! Thanks for all your comments today, I’ll let the other bloggers know so the person who wrote the article can give you a reply 🙂

      As for the evolution of photolyases, I actually don’t know masses of detail about this. Photolyases are found throughout bacteria, and were found in placental mammals until the gene was lost (this essentially happens by accident all of the time, and is how evolution as a concept works- but because we have other repair pathways the loss of the photolyases wasn’t a problem). We do have a very similar type of protein called cryptochromes which looks very similar and works in a similar way, but cryptochromes don’t repair DNA, instead they have roles in regulating our biological clock and has been linked to animals being able to sense magnetic fields (so potentially how animals find their way home when they migrate). There is still so much we don’t know about the proteins though (or at least I haven’t read!)

      As to your other comment- mutations can arise from a number of exogenous agents (things from outside of the body like UV, chemicals, radiation, etc) or endogenous agents (things within the body that are naturally produced but which must be properly disposed of, such as reactive oxygen species). These cause different DNA lesions, in the case of UV damage this is in the form of DNA dimers where instead of bases pairing up between the two strands that make up the DNA helix, bases will instead make a bond with the base next to them on the same helix. This forms a bulge in the DNA helix and when we try to replicate our DNA (when cells are going to divide) the DNA polymerase gets stuck- if the lesion isn’t repaired then you end up with the new DNA having a gap in it where the polymerase has nothing to read from. If we then try to fill in this gap with a random base it could be the wrong one, which is a mutation in the DNA. There are lots of ways that this occurs with different DNA damaging agents- sometimes bases are modified which causes them to look like another base, so the polymerase inserts the wrong base in the new strand it is synthesising. Essentially with any DNA damage, if it’s not fixed before the DNA polymerase tries to replicate the DNA then the mutation becomes “fixed” in the newly synthesised strand as we have no way of recognising that it is incorrect.

      It’s all a bit complex and quite hard to explain, so if you want any more information let me know and I’ll try and explain a bit better!


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