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The UV components of sunlight are believed to be a major cause of human skin cancer, and DNA is thought to be the principal molecular target. Alterations of the intensity and wavelength distribution of solar UV radiation reaching the surface of the earth, for example by depletion of stratospheric ozone, will change the effectiveness of solar radiation in damaging DNA in human skin. Evaluation of the magnitude of such effects requires knowledge of the altered sunlight spectrum and of the action spectrum for damaging DNA in human skin. We have determined an action spectrum for the frequency of pyrimidine dimer formation induced in the DNA of human skin per unit dose of UV incident on the skin surface. The peak of this action spectrum is near 300 nm and decreases rapidly at both longer and shorter wavelengths. The decrease in our action spectrum for wavelengths <300 nm is attributed to the absorption of the upper layers of the skin, an in situ effect that is inherently included in our measurements. Convolution of the dimer action spectrum with the solar spectra corresponding to a solar angle of 40' under current levels of stratospheric ozone (0.32-cm 03 layer) and those for 50% ozone depletion (0.16-cm 03 layer), indicate about a 2.5-fold increase in dimer formation. If the action spectrum for DNA damage that results in skin cancer resembles that for dimer induction in skin, our results, combined with epidemiological data, suggest that a 50% decrease in stratospheric ozone would increase the incidence of nonmelanoma skin cancers among white males in Seattle, Washington, by 7.5-to 8-fold, to a higher incidence than is presently seen in the corresponding population of Albuquerque, New Mexico.Sunlight causes erythema, premature aging, and cancers in human skin (1), and several lines ofevidence indicate that UV radiation of wavelengths <320 nm is of primary importance in damage induction (2). Studies of the wavelength dependence of carcinogenesis in mouse skin (3) and of erythema induction in human skin (4) indicate that the efficiency of damage induction by photons in the wavelength range 290-400 nm varies strikingly. Thus, alteration of the solar spectrum reaching the earth's surface-for example, through alteration in the ozone content of the stratosphere-will affect the frequency of DNA damages, including those in human skin.Quantitative prediction of the extent of damage and of its biological consequences requires convolution of the altered solar spectrum with the action spectrum for inducing human skin cancer (2). Because this action spectrum is not known, other biological response functions have been used to approximate the human skin cancer spectrum: action spectra (i) for carcinogenesis in mouse skin (3), (ii) for killing and mutation in prokaryotes (2), and (iii) for killing, mutation, and transformation of mammalian cells in culture (5, 6), as well as several different action spectra (iv) for erythema in human skin (4, 7). However, the optical properties of mouse skin and of prokaryotes and mammalian ...

The time-resolved fluorescence properties of phenol and straight-chained phenol derivatives and tyrosine and simple tyrosine derivatives are reported for the pH range below neutrality. Phenol and straight-chained phenol derivatives exhibit single exponential fluorescence decay kinetics in this pH range unless they have a titratable carboxyl group. If a carboxyl group is present, the data follow a two-state, ground-state, Henderson-Hasselbalch relationship. Tyrosine and its derivatives with a free carboxyl group display complex fluorescence decay behavior as a function of pH. The complex kinetics cannot be fully explained by titration of a carboxyl group; other ground-state processes are evident, especially since tyrosine analogues with a blocked carboxyl group are also multiexponential. The fluorescence kinetics can be explained by a ground-state rotamer model. Comparison of the preexponential weighting factors (amplitudes) of the fluorescence decay constants with the 1H NMR determined phenol side-chain rotamer populations shows that tyrosine derivatives with a blocked or protonated carboxyl group have at least one rotamer exchanging more slowly than the radiative and nonradiative rates, and the fluorescence data are consistent with a slow-exchange model for all three rotamers, the shortest fluorescence decay constant is associated with a rotamer where the carbonyl group can contact the phenol ring, and in the tyrosine zwitterion, either rotamer interconversion is fast and an average lifetime is seen or rotamer interconversion is slow and the individual fluorescence decay constants are similar.