It seems odd that beachgoers who toast themselves in the sun notice only when they return home hours or even days later that their skin has changed color and become tanned.
A new Tel Aviv University (TAU) study has uncovered the science behind the mystery of why the body’s tanning process doesn’t show up immediately after sun exposure. They found that the body’s initial response is to give priority to repairing DNA damage in the skin cells that inhibits the mechanism responsible for tanning.
Only after the cells have repaired the genetic information to the best of their ability do they begin to produce the increased amounts of the pigment named melanin that darkens the skin, which generates physical protection for the genetic material in the cell, protecting against the next radiation exposure.
Interestingly, independent of sun exposure, DNA damage can directly induce delayed pigmentation. For example, chemotherapy may induce hyperpigmentation in cancer patients few weeks after treatment initiation. In contrast, the UV radiation stress response occurs immediately after exposure, involving DNA repair, inflammation, and immune system recruitment.
Why does your skin not change color immediately after tanning?
The study was published in the Nature Group’s Journal of Investigative Dermatology under the title “ATM signaling delays skin pigmentation upon UV exposure by mediating MITF function towards DNA repair mode.” It was led by doctoral student Nadav Elkoshi and Prof. Carmit Levy of the human molecular genetics and biochemistry department at TAU’s Faculty of Medicine, and in collaboration with a number of other TAU researchers and colleagues from the Wolfson Medical Center in Holon, the Weizmann Institute of Science in Rehovot, the University of California, and Paris-Saclay University.
To test their hypothesis, the team activated the DNA repair mechanism in both animal models and human skin tissues. A tan developed even without any exposure to UV radiation, substantiating their findings.
“The genetic information must be protected from mutations, so this repair mechanism takes precedence inside the cell during exposure to ultraviolet radiation from the sun. The DNA repair mechanism essentially tells all the other mechanisms in the cell, ‘Stop everything, and let me work in peace.’ One system effectively paralyzes the other, until the DNA correction reaches its peak, which occurs a few hours after the UV exposure,” said Levy.
“Only then does the pigment production mechanism get to work. In our previous research, we showed that a protein called MITF, which is activated during exposure, is responsible for regulating these two mechanisms. In the current study we show that another protein, called ATM, which plays a key role in DNA repair, activates one mechanism while disabling the other. This process likely harnesses the pigmentation mechanism’s components to maximize the chances of the cell surviving without mutations following radiation exposure,” she continued.
“This scientific discovery has revealed a molecular mechanism that could serve as a foundation for further research that may lead to innovative treatments that will provide maximum protection of the skin against radiation damage; in the long run, it may even contribute to the prevention of skin cancer,” Levy concluded.
