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ACTION SPECTRA FOR INACTIVATION OF NORMAL and XERODERMA PIGMENTOSUM HUMAN SKIN FIBROBLASTS BY ULTRAVIOLET RADIATIONS
Author(s) -
Keyse S.M.,
Moss S. H.,
Davies D. J. G.
Publication year - 1983
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.1751-1097.1983.tb04478.x
Subject(s) - xeroderma pigmentosum , pyrimidine dimer , action spectrum , fibroblast , ultraviolet , dna , lesion , wavelength , strain (injury) , dna damage , human skin , complementation , nucleotide excision repair , biophysics , chemistry , microbiology and biotechnology , biology , in vitro , phenotype , genetics , biochemistry , optoelectronics , materials science , pathology , medicine , anatomy , gene
—Action spectra for UV‐induced lethality as measured by colony forming ability were determined both for a normal human skin fibroblast strain (lBR) and for an excision deficient xeroderma pigmentosum strain (XP4LO) assigned to complementation group A using 7 monochromatic wavelengths in the range 254‐365 nm. The relative sensitivity of the XP strain compared to the normal skin fibroblasts shows a marked decrease at wavelengths longer than 313 nm. changing from a ratio of about 20 at the shorter wavelengths to just greater than 1.0 at the longer wavelengths. The action spectra thus indicate that the influence on cell inactivation of the DNA repair defect associated with XP cells is decreased and almost reaches zero at longer UV wavelengths. This would occur, for example, if the importance of pyrimidine dimers as the lethal lesion decreased with increasing wavelength. In common with other studies both in bacterial and mammalian cells, our results are consistent with pyrimidine dimers induced in DNA being the major lethal lesion in both cell strains over the wavelength range 254‐313 nm. However, it is indicated that different mechanisms of inactivation operate at wavelengths longer than 313 nm.