Researchers from Tel Aviv University have put forth a novel idea to explain why the body’s tanning process takes several hours or even days to begin following exposure to the sun’s rays.
According to the study, the body prioritizes repairing DNA damage in skin cells as its primary response to sun exposure, which prevents the mechanism that causes skin pigmentation, or “tanning,” as it is widely known. Researchers from the Wolfson Medical Center in Holon, the Weizmann Institute of Science in Rehovot, the University of California, and Professor Carmit Levy of the Department of Human Molecular Genetics and Biochemistry at the university’s Faculty of Medicine led the study, which was published in the Journal of Investigative Dermatology.
We have two systems in place to shield the skin from harmful UV radiation. The first mechanism includes the repair of DNA in radiation-damaged skin cells, and the second involves enhanced melanin production, which darkens the skin in order to shield it from further radiation exposure, according to Elkoshi.
It turns out that the pigmentation mechanism is momentarily inhibited because the DNA repair mechanism takes precedence over all other systems in the cell. Only once the cells have done their best to repair the genetic information do they start to generate more melanin,” he continued.
The researchers turned on the DNA repair system in both animal models and human skin tissues to verify their theory.
Both individuals obtained tans despite not being exposed to UV rays, supporting their findings.
This repair mechanism takes precedence inside the cell during exposure to UV radiation from the sun since the genetic information needs to be safeguarded against mutations, according to Levy. “The DNA repair mechanism essentially instructs all other cell mechanisms, ‘Stop everything and let me operate in peace.’
One system completely paralyzes the other until the DNA correction reaches its peak, which happens a few hours after the UV exposure. She explained that the pigment synthesis mechanism doesn’t start working until after that.
The scientists have previously demonstrated that these two systems are controlled by a protein called MITF, which is active after exposure. Another protein known as ATM was discovered in the current study.
It is essential for DNA repair and activates one pathway while inhibiting the other.
The pigmentation mechanism’s components are probably used in this process to increase the likelihood that the cell can survive radiation exposure without mutating, according to Levy.
The discovery will act as a springboard for additional study that may result in cutting-edge therapies offering the skin the maximum protection against radiation damage and, in the long run, may help prevent skin cancer.
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