Sun worshippers may someday slather on an after-suntan lotion that repairs some of the genetic damage caused by ultraviolet (UV) light. According to researchers in Germany and the Netherlands, a compound under study that contains a DNA-repairing enzyme may allow sunburn sufferers to reverse some skin-cell mutations that can later become cancer.

The treatment reduced a key sign of skin damage by 40% to 45% among 19 study volunteers who were exposed to UVB radiation long enough to get a mild burn.

The lotion could allow people to not only prevent burns with conventional sunscreens, but to also perform damage control after burns occur. Exposure to the sun's rays can harm DNA in skin cells, which can lead to cancer. Such DNA mutations often include lesions called pyrimidine dimers; researchers believe these lesions contribute to cancer by damaging tumor-suppressing genes and by hindering the immune system's response to sunburn.

The researchers took aim at dimers with a lotion containing a DNA-repairing enzyme called photolyase. Found in many primitive organisms and certain higher life forms such as fish, photolyase is activated by light and specifically targets and removes pyrimidine dimers from DNA.

Human skin has its own DNA-repair system, but whether it can sustain such a light-activated photolyase response is still not certain, Stege's team reports. The recent discovery of a human version of a photolyase gene has "raised the possibility" that photolyase therapy could help sun-damaged human skin, the researchers explain. The current study looked at a lotion with photolyase derived from plankton.

After exposing the study participants to enough UVB exposure to cause mild burns, the researchers found significant numbers of pyrimidine dimers in their skin cells. Subjects were immediately treated with the lotion, and one hour later were exposed to light waves in order to activate the photolyase. Treatment cut skin-cell dimers by up to 45%. In contrast, the researchers note, no reduction was seen in additional experiments using lotion without photolyase or using light therapy before applying the lotion.

By removing dimers from skin-cell DNA, the lotion also completely prevented the suppression of two immune responses that help repair sun damage, the investigators report. In untreated UVB-exposed skin, however, these responses were inhibited.

Because these immune responses were protected by only partially removing dimers from sun-damaged skin cells, it may not be necessary to completely rid DNA of dimers for the treatment to work, the authors note. They speculate that a certain number of dimers might have to be present to override immune responses.

Proceedings of the National Academy of Sciences February 15, 2000;97:1790-1795