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DOSE‐RESPONSE OF CHRONIC ULTRAVIOLET EXPOSURE ON EPIDERMAL FORWARD SCATTERING‐ABSORPTION IN SK‐1 HAIRLESS MOUSE SKIN
Author(s) -
Menter Julian M.,
Acin Patricia P.,
Sayre Robert M.,
Willis Isaac
Publication year - 1992
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1992.tb08514.x
Subject(s) - hairless , stratum corneum , chemistry , action spectrum , irradiation , wavelength , molar absorptivity , chromophore , excitation , ultraviolet , absorption (acoustics) , photochemistry , biophysics , optics , physics , pathology , medicine , biochemistry , biology , quantum mechanics , nuclear physics
— This work provides a dose‐response model of UV‐induced epidermal‐stratum corneum thickening induced by irradiation at wavelength X. This model assumes that photobiochemical reaction(s) can give rise to hyperplasia in a manner which is predictable from a simple photochemical kinetic scheme. In this work, we derive an equation which predicts an approximately linear relationship between the logarithm of the increase in optical skin thickening measured at 320 nm (ΔOD 320 ) and total cumulative dose (D T ) seen by the target cells in or near the basal layer. For each excitation wavelength Λ, the slope R(Λ) of the log ΔOD 320 vs D T plot is proportional to ε(Λ) φ rx where ε(Λ) is the extinction coefficient for the target chromophore at excitation wavelength, and φ rx is the quantum yield for the photochemical reaction(s) leading to hyperplasia. Our data previously obtained from irradiation of SK‐1 hairless mice with “monochromatic” UV wavebands at 280, 290, 300, 307 and 313 nm (Menter et al. , 1988, Photochem. Photobiol. 47, 225–260.) and data from Sterenborg and van der Leun at 254 and 313 nm (1988, Photodermatology 5, 71–82) are in good agreement with this model, except for 254 and 280 nm excitation, which are greatly attenuated by epidermis‐stratum corneum. For excitation at the latter wavelengths, “dark” regressive processes successfully compete with the “light” reaction(s) which lead to (pre)cancerous lesion. This difficulty notwithstanding, the “intrinsic” action spectrum for hyperplasia derived from these measurements indicates that the target chromophore preferentially absorbs in the UV‐C region. Assuming ε(Λ) ≅ 1000 M ‐1 cm ‐1 of 280 nm, our values of R(Λ) indicate that the photochemical reaction(s) leading to hyperplasia are roughly as efficient as thymine photodimerization in aqueous solution, with φ rx ≅ 4 × 10– 4 . This work is important because it illustrates that, to a first approximation, even complex photobiological processes may be rationalized on the basis of fundamental photochemical processes, as occurring in “simple” homogeneous photochemical reactions in solution.