"Moving immediately into the shade does not stop sun damage, as UV rays can continue damaging skin cells hours after exposure," The Guardian reports. A study has found evidence that damage to DNA can continue after initial exposure…
"Moving immediately into the shade does not stop sun damage, as UV rays can continue damaging skin cells hours after exposure," The Guardian reports. Ultraviolet (UV) light is known to cause damage to DNA in skin cells, which increases the risk of the most serious type of skin cancer: melanoma.
This study aimed to examine the biological mechanisms that may be involved in this process.
Researchers used pigment-producing skin cells from mice (melanocytes) and found that it is the pigment melanin that plays a role in the damage process.
Exposure to UV light causes melanin to produce small molecules, called cyclobutane pyrimidine dimers (CPDs). The CPDs form abnormal bonds between the "building blocks" in the DNA helix. These CPDs are formed at the time of UV exposure, but the research showed that the formation of CPDs also continues for three or more hours after UV exposure has stopped ("after dark"). After this, DNA repair mechanisms step in.
Some tests using human melanocytes were also performed. This was said to similarly demonstrate the continued formation of CPDs after dark, but the effects were much more variable. It is unclear whether the situation in humans is completely identical.
Overall, the findings reinforce the risks of over-exposure to sunlight. It is easy to forget that the sun is a giant nuclear fusion reactor that emits radiation. Therefore, it is important to be sun-smart to reduce your risk of skin cancer.
You don’t need to get a suntan, let alone sunburn, to harvest the vitamin D-boosting effect of sunlight.
The study was carried out by researchers from Yale University School of Medicine in the US and other institutions in Brazil, Japan and France. The study was supported by various grants, including those from the Department of Defence and National Institutes of Health.
The study was published in the peer-reviewed scientific journal Science Magazine.
The UK media’s reporting of the study was accurate, though some of the headlines were potentially confusing. For example, headlines such as The Daily Telegraph’s “Sunlight damages DNA even in the dark” and The Guardian’s “Exposure to sun poses risk of skin cancer even in the dark” could be taken the wrong way. People may be concerned that when they go out at night, the sun is damaging their skin and they need to cover up. The results of the study actually suggest that the damage caused by UV exposure to the skin continues for some hours after the exposure has stopped (e.g. after you have come in for the evening, after a day at the beach).
This was a laboratory study aiming to see by what processes UV light causes damage to the DNA in skin cells.
Melanin is the pigment in skin and hair cells, which is present in variable amounts across individuals. The amount and type of pigment in your skin, such as pheomelanin and eumelanin, are associated with the risk of developing melanoma – the most serious type of skin cancer.
People with blonde and red hair have higher amounts of yellow pheomelanin relative to brown eumelanin in their skin and hair, which puts them at higher risk than people with darker skin and hair.
Previous research has demonstrated that when melanin, particularly yellow pheomelanin, is exposed to UV light, this produces reactive oxygen species (ROS) – molecules that can cause cell damage and "breaks" in the DNA. Looking at the DNA abnormalities present in melanoma, it seems that in most cases there are distortions to the DNA helix. This is due to the presence of molecules called cyclobutane pyrimidine dimers (CPDs), which cause abnormal bonds between the “building blocks” in the DNA.
Ultraviolet A type radiation (UVA) makes up around 95% of the UV entering the atmosphere. However, the researchers say that although UVA is clearly linked to melanoma, UVA is not very good at making these CPDs directly. The researchers therefore aimed to look at the biochemical pathways that cause the pigment-producing skin cells (melanocytes) to produce CPDs.
The researchers carried out a variety of laboratory experiments, where melanocytes from mouse and human skin were exposed to UVA and UVB light. They used special laboratory techniques to examine the DNA in the cells, looking for the generation of CPDs at the time of UV exposure and for some time after UV exposure had been discontinued (“after dark”).
The researchers then carried out further studies to see what biochemical processes may be causing the melanocytes to produce CPDs.
The researchers showed that exposure to UVA light causes the immediate production of CPDs. Unexpectedly, CPD generation continued for three or more hours after UVA exposure was stopped. After this, the formation of CPDs was offset by DNA repair mechanisms.
Experiments using melanocytes from albino mice suggested that it was the melanin pigment that was involved in the continued production of CPDs after dark, as pigment-free melanocytes did not continue to produce CPDs after UVA had been stopped.
Half of all CPDs produced after UVA exposure to mouse melanocytes were found to be formed in this “after dark” period, when exposure had stopped. Further tests with UVB light showed that most of the CPDs produced occurred after dark. Further tests in the mice suggested that the red-yellow pigment pheomelanin is both a “poorer shield” against the generation of CPDs at the time of UV exposure, and a stronger generator of CPDs after dark.
Tests with the human melanocytes similarly demonstrated the production of CPDs after dark, but in human cells the response was said to be much more variable. The researchers considered that this could be due to genetic differences, though they could not look into this further due to privacy restrictions on the donated skin.
When looking into the underlying biochemical pathways involved in the production of CPDs after dark, they found that this was due to UV-induced reactive oxygen and nitrogen species combining and causing excitation (the application of energy) of an electron in the melanin pigment. The energy produced during this process is transferred to the DNA and causes the formation of CPDs.
The researchers conclude that pigment-producing skin cells (melanocytes) cause the production of “dark CPDs”, even after UV exposure ends. They say that melanin, while it may protect against cancer in one respect (e.g. people with darker skin having lower risk), it may also be cancer-causing (carcinogenic).
They also say that their findings “validate the long-standing suggestion that chemically generated excited electronic states are relevant to mammalian biology”.
This laboratory research examined the biochemical processes by which UV exposure causes damage to the DNA in skin cells, and so increases the risk of melanoma.
The research which used mouse pigment cells in the laboratory, confirmed that the melanin pigment plays a role. Exposure to UV light causes melanin to produce CPD molecules, which cause abnormal bonds to form between the “building blocks” in the DNA helix. The research showed that the formation of CPDs continues for three or more hours after UV exposure has stopped (“after dark”) before DNA repair mechanisms step in. The melanin pigment is necessary for the continued formation of CPDs after dark (pigment-free cells did not do this), and there was also the suggestion that different types of melanin could have differing effects. For example, the red-yellow pigment pheomelanin seemed to be a stronger generator of CPDs after dark.
However, it should be noted that most of these results came from experiments using mouse pigment cells. Although UV exposure to human melanocytes was said to similarly cause the continued formation of CPDs after dark, the effects were reported to be much more variable. The researchers considered that this could be due to genetic differences, but they were not able to explore this further, due to privacy restrictions.
Therefore, these results must be predominantly considered to be applicable to mice. Although this is likely to be a good indication of the biochemical pathways that may occur in human skin cells after UV exposure, it is not know if the results would be completely identical.
Overall, the findings show that at whatever time UV exposure causes most damage to the skin – either at the time of exposure, or in the continuing hours afterwards – it does cause DNA damage to the skin, which is linked to the risk of skin cancer. The study again highlights the importance of safety in the sun, including the use of sunscreen, sunglasses and skin coverage.