ACTION SPECTRA FOR THE INDUCTION OF PYRIMIDINE(6‐4)PYRIMIDONE PHOTOPRODUCTS AND CYCLOBUTANE PYRIMIDINE DIMERS IN NORMAL HUMAN SKIN FIBROBLASTS

Abstract. Normal human skin fibroblasts were exposed to 265–313‐nm monochromatic UV wavelengths and the yield of pyrimidine(6‐4)pyrimidone photoproducts [(6‐4) photoproducts] and cyclobutane pyrimidine dimers (dimers) measured by radioimmunoassay. The action spectra for the induction of these two types of DNA damage were very similar for wavelengths from 254 to 302 nm. However, the action spectrum value for (6‐4) photoproduct production was less than half the value obtained for dimer induction by 313‐nm UV. Cells were also exposed to the UV produced by a broad‐spectrum fluorescent sunlamp (280–360 nm, peak at 313 nm) under conditions in which various wavelength components were removed from the spectrum. For exposures in which the (6‐4) photoproducts and dimers were induced primarily by wavelengths shorter than 310 nm, their rates of induction, relative to 254‐nm‐irradiated cells, were similar. However, the level of (6‐4) photoproduct production was about three‐fold lower than dimer induction for sunlamp irradiations in which the 315–330‐nm component of this source was primarily responsible for the formation of this damage. These results are consistent with the conclusion that for treatments in which (6‐4) photoproducts are produced by wavelengths in the 310–320‐nm range, which represent the region of absorption peaks for these photoproducts, both the induction and photolysis of (6‐4) photoproducts occur simultaneously during irradiation.