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DNA Lesions and Mammalian Cell Killing: Cause and Effect?
Author(s) -
Elkind M. M.,
BenHur Ehud
Publication year - 1972
Publication title -
israel journal of chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.908
H-Index - 54
eISSN - 1869-5868
pISSN - 0021-2148
DOI - 10.1002/ijch.197200128
Subject(s) - dna damage , dna repair , chemistry , dna , bromodeoxyuridine , cell , microbiology and biotechnology , dna damage repair , lesion , cell division , biophysics , cell growth , biochemistry , biology , pathology , medicine
Although indirect, studies of repair mechanisms afford a useful approach to the questions: Where and what are the sensitive sites in a cell related to division? This approach has been used with mammalian cells based on the fact that sublethal damage must be accumulated to kill a cell and the observation that cells can repair sublethal damage. Actinomycin D was found to inhibit this repair, an observation which justified a focus upon nuclear DNA as the site of damage and repair. Sedimentation studies with alkaline gradients revealed two repair processes. Repair of single‐strand breaks (also found by others) and repair to a complex of DNA, lipid, and protein. In cells sensitized to fluorescent light because of prior growth in the presence of 5‐bromodeoxyuridine, the data suggest that single‐strand breaks is the lethal lesion. In contrast, damage to a DNA‐membrane structure appears a more likely target for X‐ray cell killing.