Your skin's response to Sun exposure may seem delayed, but there's a good reason for it, scientists have found.
Through experiments on both human and mouse skin, a team led by molecular biologist Nadav Elkoshi of Tel Aviv University in Israel has discovered that the development of a tan only occurs after the skin has taken care of emergency DNA repair.
"We have two mechanisms designed to protect the skin from exposure to dangerous UV radiation," Elkoshi explains.
"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."
Elkoshi and his team hypothesized that the delay in tanning is a result of resource prioritization. Basically, all of the cell's resources mobilize to repair radiation damage as quickly as possible. It's only once that task is complete that the cell can allocate resources to the production of melanin.
To test this hypothesis, the researchers first exposed human skin, obtained from consenting surgery patients and cultured in petri dishes, to UVB radiation. This was so that they could study the activity in the cell in response to radiation damage.
They confirmed that a protein kinase called ATM, activated by DNA damage and critical to cell repair, springs into action shortly after exposure to UVB radiation. That's interesting, but the team needed more information.
So, the follow-up step was to trigger the activation of ATM in the absence of UVB exposure and observe the results. This phase of the experiment was conducted on mouse models, and more human skin samples in petri dishes. In both mouse and human skin, a tan developed after an interval, even in the absence of harmful radiation.
A close inspection of the cellular processes involved showed that the activation of ATM blocks the activation of the MITF protein responsible for increasing melanin production, so that DNA repair can take precedence.
"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," explains Carmit Levy, a biochemist and molecular biologist at Tel Aviv University.
"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."
The team suspects that DNA repair may even harness some of the components of the pigmentation mechanism in order to maximize the chances of cell survival, and minimize the chances of mutation.
The discovery, the team says, could be used to help study, understand, prevent, and treat the effects of skin radiation damage.
"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," Levy says.
"In the long run, it may even contribute to the prevention of skin cancer."
The research has been published in the Journal of Investigative Dermatology.