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SUNLIGHT‐INDUCED KILLING OF NONDIVIDING HUMAN CELLS IN CULTURE
Author(s) -
Kantor G.J.,
Ritter C.
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.tb04514.x
Subject(s) - pyrimidine dimer , sunlight , dna damage , programmed cell death , cell , irradiation , dimer , cell culture , dna , biology , microbiology and biotechnology , biophysics , chemistry , biochemistry , apoptosis , genetics , optics , physics , organic chemistry , nuclear physics
Nondividing populations of human diploid fibroblasts that are DNA excision repair proficient (WS‐1, KD. SSCW) and repair deficient (XP12BE) were exposed to mid‐day summer sunlight for a determination of survival based on an ability of cells to remain attached to a culture vessel surface. Whereas mid‐ and far‐UV wavelengths and radiation emitted from a sunlamp cause a gradual degeneraton and detachment of cells in a dose‐dependent manner, sunlight does not promote cell killing that is evidenced by these criteria in repair proficient cells. Detachment of repair deficient cells is promoted to a limited extent but only at sunlight exposure times that are low with respect to the amount of DNA damage (pyrimidine dimers) induced. Repair proficient and deficient cells exposed to sunlight for longer times do not detach but are incapable of excuding a viable stain several days after exposure and appear as histologically fixed cells. Pyrimidine dimer levels in these sunlight irradiated cells were great enough to have promoted detachment had these levels been induced by UV (254 nm) alone. Other photodamage induced by these exposures evidently inhibits the dimer‐induced cell degeneration that leads to cell detachment. We conclude that pyrimidine dimers are responsible for cell killing at short sunlight exposure times (< 40 min) but that at longer exposures (> 80 min) cells arc killed by a different mechanism that is independent of dimer‐caused death.