Studies show DNA damage by long UV.

Warnings about the sun's burning, aging and potentially carcinogenic rays are usually directed againat overexposure to a portion of the ultraviolet (UV) spectrum termed UV-B--the medium-length UV wavelengths ranging from about 250 to 320 nanometers. For decades scientists believed longer-wave UV radiation had little biological effect. But research at Argonne (Ill.) National Laboratory is now demonstrating clearly identifiable damage to DNA--both in bacteria and in human cells--irradiated with the longer wavelengths known as UV-A. Moreover, this research is showing that the mechanisms causing UV-A's damage is quite different from what occurs with exposure to shorter UV wavelengths.

The importance of UV-A-caused DNA damage has not been determined, says Argonne group leader Meyrick Peak. Though long UV produces DNA damage with only perhaps 1/1,000 the efficiency of mid-range UV-B, he points out that UV-A penetrates light-colored skin more deeply than UV-B does. "So my feeling is that the [longwave UV-A] might prove important in the formation of skin damage," he told SCIENCE NEWS.

Shorter UV wavelengths--in the B and C portions of the spectrum--will damage DNA directly. According to Peak, "The DNA of the cells absorbs far UV [UB-B and -C] very strongly," transferring the photons' energy to the electrons in the DNA. This damage is powerful "and can clearly mutate cells and cause cancer very quickly--even at low doses," he explains.

By contrast, UV-A's effect on DNA are indirect. "DNA doesn't absorb near-UV [UV-A] as far as we can tell," Peak says. However, his group has identified cellular chemicals, which they call sensitizers, that do absorb that UV-A's photon energy. This absorption excites, or raises the energy level of, the sensitizers' electrons. But even they do not damage DNA, it appears. That's oxygen's role.

"We believe that these excited sensitizers can transfer energy directly to molecular oxygen," creating powerful, chemically reactive oxygen species, write Meyrick Peak and his wife, biochemist Jennifer Peak, in the latest (autumn) issue of LOGOS, an Argonne publication. These reactive oxygen species quickly decay to molecular oxygen by releasing their excess energy. If they decay near DNA, they can damage it.

Their data show that when cells are irradiated in oxygen-free environments, virtually no UV-A damage occurs. However, when those name cells are irradiated in water (as they naturally would be in the body), eight different types of DNA damage will occur. And irradiation of cells in "heavy" water (where the hydrogen is substituted with deuterium) yields almost twice as much DNA damage. The reason, the Peaks believe, is that since reactive oxygen decays more slowly in heavy water, it has more time to diffuse into the vicinity of a DNA molecule.

Most recently, the Peaks have added porphyrin (a constituent of hemoglobin), bilirubin and riboflavin (vitamin B.sub.2.) to a growing list of sensitizer molecules, and identified superoxide anion (O.sub.2.) as one of the reactive oxygen species. According to biologist Richard Setlow, acting directory of life sciences at Brookhaven National Laboratory in Upton, N.Y., they also "have probably done the best work in trying to sort out what are the various [DNA changes] due to UV-A."

"For 60 or 70 years, it was felt that longwave UV radiation had very little if any biological effect," notes dermatologist Frederick Urbach, director of the Center for Photobiology at Temple University's Skin and Cancer Hospital in Philadelphia. In fact, he says, scientists drew the boundary between UV-A and UV-B at what they thought was the cutoff for DNA-active wavelengths. But research by the Peaks and others, using newly available lamps producing high-energy longwave UV, show that the initial UV-B cutoff of 315 to 320 nm was low, Urbach says. As a result, he expects that the boundary between UV-A and UV-B will eventually be changed to 340 nm--the point at which longer wavelengths cause almost entirely those indirect, oxygen-mediated DNA effects.