The time of exposure to UV radiation might influence the onset of skin cancer in mice, according to a study.

Exposure to UV radiation triggers DNA lesions that can lead to skin cancer.

Previous studies in mice have shown that levels of a protein called XPA--involved in repairing UV-induced DNA lesions--waxes and wanes with the time of day, peaking between 4-6 p.m. and dipping between 4-6 a.m. in tune with the circadian clock. Aziz Sancar and colleagues found that in mouse skin cells the protein's level and activity are at their lowest at 4 a.m. and at their highest at 4 p.m.

The authors exposed two groups of mice to UV radiation—one at 4 a.m. and the other at 4 p.m.—and monitored the onset of skin cancer. Mice irradiated when the repair activity was at its lowest developed tumors much faster and at five-fold higher frequency compared with mice exposed to UV when the protein's repair function was at full throttle.

When the authors repeated the experiment in a strain of mice lacking two key components of the circadian clock, the time of UV exposure tracked neither the protein's repair activity nor the onset of skin cancer, suggesting that circadian control of the XPA protein might influence skin cancer rates. B

ecause mouse and human circadian clocks are similar, the time of UV exposure might likewise determine its cancer-causing potential in people, according to the authors.

Source: UNC