Sunbathers can experience cancer-causing DNA damage up to three hours after they've left the beach or the tanning bed, according to a new study.
Surprisingly, this delayed response takes place in cells containing the skin pigment melanin, which is usually thought to block harmful ultraviolet radiation in skin. In these cells, UV radiation sets in motion a chemical chain reaction that causes DNA damage in these cells.
Yale Professor Douglas Brash discusses the new research on melanin and skin cancer. | Yale University
"What's a surprise here is that melanin is doing things that could actually cause cancer as well as prevent it," said study author Douglas Brash of Yale University. "You're getting the same kinds of DNA damage in your skin for hours after the sunlight exposure has ended."
The study by Brash and colleagues appears in the 20 February issue of Science.
Their findings may be particularly important as the most aggressive type of skin cancer, called melanoma, is on the rise globally. In the United States, melanoma cases have been increasing by about 2% per year, as more people use tanning beds and increase their time in the sun by using sunscreens.
UV radiation causes breaks or lesions in skin cell DNA as the DNA absorbs UV photons, and it's these lesions that lead to cancer-causing mutations. The lesions, called cyclobutane pyrimidine dimers or CPDs, usually appear within less than a second after UV radiation exposure.
When Brash and his colleagues looked closer at UV damage in mouse and human cells, however, they discovered a whole other group of CPDs that occur in melanin-producing cells. These "dark" CPDs appear hours after exposure to UV radiation, they found.
The scientists traced out a complicated pathway for the production of dark CPDs. First, UV radiation produces several types of reactive oxygen and nitrogen that break down melanin into granules. These fragments contain a high-energy electron, and the energy released from these fragments can damage DNA somewhat like a UV photon would.
The researchers suggest that there may be a way to develop sunscreens for use after exposure that tamp down on this high-energy state and prevent the buildup of dark CPDs. This "after-dark" sunscreen might contain one of several kinds of agents, they said.
For instance, Brash said that antioxidants like vitamin E might prevent the oxygen and nitrogen reactions from starting or reverse the chemical steps that occur after the start of the reaction but before the high-energy state. Other agents like ethyl sorbate used after UV exposure could "dissipate the energy to heat before it can go to DNA," he suggested.
"However, if sorbate is present during UV exposure, it also diverts energy to DNA, so it is not the safest thing to put in a sunscreen," Brash said. "We'd want chemicals similar to sorbate but having lower energies."
These antioxidants or energy-quenching compounds would have to get into skin cells, and there isn't much published evidence about whether antioxidants in pills or those already contained in sunscreen ever make it into cells, Brash said.
"In talking to chemists, there are broad predictions but each compound needs to be tested experimentally," he concluded.