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REPAIR OF NEAR‐VISIBLE‐ and BLUE‐LIGHT‐INDUCED DNA SINGLE‐STRAND BREAKS BY THE CHO CELL LINES AA8 and EM9
Author(s) -
Churchill Mark E.,
Peak Jennifer G.,
Peak Meyrick J.
Publication year - 1991
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.1751-1097.1991.tb02068.x
Subject(s) - chinese hamster ovary cell , biology , dna repair , microbiology and biotechnology , cell culture , dna , genetics
The induction of single‐strand breaks (SSB) and the kinetics of SSB repair were measured in two Chinese hamster ovary cell lines irradiated with monochromatic photons of near‐visible radiation (405 nm) and blue light (434 nm). The radiosensitive and UV‐A‐sensitive mutant line EM9 is known to repair SSB induced by ionizing radiation or 365‐nm UV‐A more slowly than the parent line AA8. At the 10% survival level, EM9 cells were 1.7‐ and 1.6‐fold more sensitive than AA8 cells to 405 and 434 nm radiation, respectively. This sensitivity was not due to differences in induction of SSB because AA8 and EM9 cells accumulated the same number of initial breaks when irradiated at 0.5°C with either 405 nm (5.9 SSB per MJ/m 2 ) or 434 nm (5.1 SSB per MJ/m 2 ), as measured by alkaline elution. When the cells repaired these SSB at 37°C in full culture medium, biphasic repair kinetics were observed for both cell lines. In both phases of repair, EM9 cells repaired breaks induced by both wavelengths more slowly than did AA8 cells. The 1 ½ values for the repair phases for 405‐nm‐induced SSB were 3.8 and 150 min for EM9, and 1.5 and 52 min for AA8; the corresponding values for repair of 434 nm breaks were 3.7 and 39 min for EM9, and 2.0 and 30 min for AA8. Because of this slower repair, EM9 cells left more SSB unrepaired after 90 min than did AA8 cells for both wavelengths. The ratio of unrepaired breaks in EM9 cells to that in AA8 cells was 1.4 and 1.7 times higher for 405 and 434 nm radiation, respectively. Thus, the sensitivity of EM9 cells to near‐visible and visible light correlates with a deficiency in repairing SSB induced by these wavelengths. These results suggest that DNA damage may be a critical event in visible‐light‐induced cellular lethality and that an important determinant of the ability of AA8 and EM9 cells to survive visible light irradiation may be their ability to repair DNA strand breaks.