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ERYTHEMA AND MELANOGENESIS ACTION SPECTRA OF NORMAL HUMAN SKIN *
459
Citations
12
References
1982
Year
Ultraviolet LightSkin ResponseUltraviolet RadiationSkin CancerPhotochemistryOphthalmologyMedicinePhotocarcinogenesisMelanomaCutaneous BiologyPathologyPhotoprotectionWound HealingBiophotonicsDermatologyCaucasian Human SkinOptogeneticsHealth Sciences
The authors measured delayed erythema and melanogenesis action spectra in untanned Caucasian volunteers for 250–435 nm by exposing skin to monochromatic radiation at varying fluences. The spectra are indistinguishable above 300 nm, similar but separated below 300 nm, with a minimum near 280 nm, a maximum near 296 nm, a steep drop between 304–334 nm, and suggest a common chromophore—likely DNA for wavelengths <313 nm—highlighting practical implications for UV skin response.
Abstract The action spectra for delayed erythema and melanogenesis in Caucasian human skin are determined for wavelengths between 250 and 435 nm. The untanned skin of very fair volunteers was observed after single exposures to a range of fluences of monochromatic radiation. At wavelengths longer than 300 nm the two action spectra are indistinguishable, and at wavelengths shorter than 300 nm, they are of similar shape despite a distinct separation. This suggests a common or similar chromophore for initiation of the vascular and pigmentary responses to UV. A broad minimum in the action spectra occurs near 280 nm, a maximum near 296 nm, and for wavelengths longer than 300 nm, increasingly larger fluences of radiation are required to induce delayed erythema and melanogenesis. Between 304 and 334 nm both action spectra exhibit a rapid decrease of almost three orders of magnitude. In contrast, between 334 and 405 nm the spectra decrease by only one order of magnitude, and there is a suggestion of a small maximum at or near 365 nm. Different chromophores, sites of damage, or response mechanisms may be responsible for induction of delayed erythema at these longer wavelengths. After spectral corrections for the optical effects of the stratum corneum, the shape and magnitude of the action spectra are grossly consistent with a mechanism in which DNA is the primary chromophore initiating the response pathways for wavelengths less than 313 nm. Whatever the actual basis for these action spectra may be, they are of practical significance in predicting skin response to sources of ultraviolet radiation.
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