The research findings reveal the mechanism behind this phenomenon, according to which the body’s initial response is to prioritize repairing DNA damage in the skin cells, which inhibits the mechanism responsible for skin pigmentation, commonly known as tanning.
They have designed two mechanisms 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 to protect it from future exposure to radiation.
In this study, they discovered why the tanning phenomenon does not occur immediately when the body is exposed to the sun, but only following a delay. 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().
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To test their hypothesis, they 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. The DNA repair mechanism essentially stops all the other mechanisms in the cell. 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. In previous research, they showed that a protein called MITF, which is activated during exposure, is responsible for regulating these two mechanisms. In the current study, they show that another protein, called ATM, which plays a key role in DNA repair, activates one mechanism while disabling the other.
The process likely harnesses the pigmentation mechanism’s components to maximize the chances of the cell surviving without mutations following radiation exposure.
This could also serve as a foundation for further research that may lead to innovative treatments that will provide maximum protection of the skin against radiation damage; it may even contribute to the prevention of skin cancer.
References:
- Luís F.Z. Batista et al. How DNA lesions are turned into powerful killing structures: Insights from UV-induced apoptosis. Mutation Research/Reviews in Mutation Research. June 2009.(https://www.sciencedirect.com/science/article/abs/pii/S1383574208001361)
- Nadav Elkoshi et al. ATM signaling delays skin pigmentation upon UV exposure by mediating MITF function towards DNA repair mode. Journal of Investigative Dermatology. May 2023.(https://www.sciencedirect.com/science/article/abs/pii/S0022202X23021243)
- Alonso-Belmonte, C et al. Current State of Skin Cancer Prevention: A Systematic Review. Situación actual de la prevención del cáncer de piel: una revisión sistemática. Actas dermo-sifiliograficas vol. 113,8 (2022): 781-791.(https://www.sciencedirect.com/science/article/pii/S0001731022003386?via%3Dihub)
Source: Eurekalert
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