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ALKALI‐LABILE LESION and URACIL‐DNA‐GLYCOSYLASE‐SENSITIVE SITE REMOVAL AFTER BrdUrd and UVB TREATMENT OF CHINESE HAMSTER CELLS *
Author(s) -
Hagan M. P.,
Matsushita T.,
Bonura T.,
Shotola A.
Publication year - 1982
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.1751-1097.1982.tb02576.x
Subject(s) - dna glycosylase , uracil , lesion , dna , uracil dna glycosylase , dna repair , kinetics , chinese hamster , cell cycle , dna damage , cell , chemistry , microbiology and biotechnology , biology , biochemistry , cancer research , pathology , medicine , physics , quantum mechanics
— A marked cell‐cycle dependency for the recovery of cells after BrdUrd/UVB treatment has led us to look for similar characteristics in the molecular events associated with DNA repair. Such characteristics are reported here for the repair of alkali‐labile lesions. When asynchronously growing cells were uniformly substituted with BrdUrd (a condition that results in the greatest cell killing), the repair kinetics followed a simple exponential response with a half‐time of approximately 17min. However, when lesions were restricted to3–5% of the genome and the repair observed in the mid‐S phase (a condition associated with sublethal damage repair), the DNA repair kinetics were complex. The rejoining of the DNA was biphasic with greater than 90% of the lesion with a half‐time of less than6–7 min. Uracil removal followed similar kinetics. Caffeine, a potent inhibitor of cell survival after BrdUrd/UVB treatment, had no measurable effect on either uracil removal or alkali‐labile lesion repair.