Tel Aviv University researchers have proposed a new theory for why the body’s tanning process does not occur immediately after exposure to the sun’s rays, but only after a few hours or even days.
The study found that the body’s initial response to sun exposure is to prioritize repairing DNA damage in the skin cells, which inhibits the mechanism responsible for skin pigmentation, commonly known as tanning.
The research, published in the Journal of Investigative Dermatology, was led by doctoral student Nadav Elkoshi and Professor Carmit Levy of the Department of Human Molecular Genetics and Biochemistry at the university’s Faculty of Medicine, and in collaboration with scientists from Wolfson Medical Center in Holon, the Weizmann Institute of Science in Rehovot, the University of California and Paris-Saclay University.
“We have two mechanisms designed to protect the skin from exposure to dangerous UV radiation. The first mechanism repairs the DNA in the skin cells damaged by the radiation, while the second mechanism involves increased production of melanin, which darkens the skin in order to protect it from future exposure to radiation,” explained Elkoshi.
“It turns out that the mechanism that repairs our DNA takes precedence over all other systems in the cell, temporarily inhibiting the pigmentation mechanism. Only after the cells repair the genetic information to the best of their ability do they begin to produce the
increased melanin,” he added.
To test their hypothesis, the researchers activated the DNA repair mechanism in both animal models and human skin tissues. In both, 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,” said Levy.
“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. Only then does the pigment production mechanism get to work,” she added.
The researchers had previously shown that a protein called MITF, which is activated during exposure, is responsible for regulating these two mechanisms. In the current study, they identified another protein, called ATM, which plays a key role in DNA repair and 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,” said Levy.
The discovery will serve as a foundation for further research that could lead to innovative treatments providing maximum protection of the skin against radiation damage and, in the long run, may contribute to the prevention of skin cancer.
