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For many a sunbather it has long been a mysterious quirk of science – why does our color only appear hours – or even days – after we leave the beach?
Now researchers claim to have the answer – and it’s because of two competing processes in our skin cells.
When exposed to the sun’s UV rays, the body’s first response is to prioritize repairing DNA damage in the cells, they claim.
But for a few hours, this response inhibits another mechanism responsible for skin pigmentation – known as tanning.
The new study was conducted by a team of biologists at Tel Aviv University in Israel, who previously found that sunbathing can boost your libido and increase your sex drive.
Beachgoers know the experience of spending hours in the sun, going home and only hours later noticing that their skin has changed color
“Skin pigmentation is paused after sun exposure, but the mechanism behind this pause is unknown,” they say in their paper, published in the Journal of investigative dermatology.
The authors explain the two mechanisms at the cellular level that protect the skin from exposure to dangerous UV radiation.
The first repairs the DNA in skin cells damaged by radiation, the second increases the production of melanin, a natural pigment in the body that also gives hair and eyes a dark color.
Melanin — produced and distributed by special cells called melanocytes — darkens the skin to protect it from future radiation exposure.
When we are exposed to UV rays, the first mechanism effectively paralyzes the other until DNA correction reaches its peak – but this happens a few hours after the UV exposure.
“The genetic information must be protected from mutations, so this repair mechanism takes precedence in the cell during exposure to ultraviolet radiation from the sun,” said study co-author Professor Carmit Levy of Tel Aviv University.
“The DNA repair mechanism essentially tells all the other mechanisms in the cell, ‘Stop everything and let me work in peace.’”
This illustration shows a cross section of the skin. Melanocytes are known for their role in skin pigmentation and their ability to produce and distribute melanin
Previous research by the team has shown that a protein called MITF, which is activated during sun exposure, is responsible for regulating the two mechanisms.
In the new study, they show that another protein called ATM, which plays a key role in DNA repair, activates the first mechanism and turns off the second.
Lab experiments on skin tissues from both mice and animals showed that ATM inhibition — in other words, removing levels of the protein — caused pigmentation.
“This process likely exploits the components of the pigmentation mechanism to maximize the chance that the cell survives without mutations after exposure to radiation,” Professor Levy said.
The team believes their study could aid future research into skin protection and ultimately help prevent skin cancer.
Manipulating how the proteins work and the interplay between the two mechanisms can better protect skin cells from DNA damage or increase pigmentation.
It is well known that exposure to UV rays from the sun and tanning beds can damage the DNA in your skin cells and cause skin cancer.
If enough DNA damage builds up over time, it can cause cells to grow out of control, which can lead to skin cancer.
This is why the NHS and other health organizations recommend applying sunscreen to the skin every two hours for optimal protection.
A type of UV radiation called UVB burns the top layers of the skin (the epidermis) and causes sunburn, while UVA radiation causes people to tan.
UVA rays penetrate to the lower layers of the epidermis, where they trigger melanocytes to produce melanin.