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ALKALI-LABILE LESION and URACIL-DNA-GLYCOSYLASE-SENSITIVE SITE REMOVAL AFTER BrdUrd and UVB TREATMENT OF CHINESE HAMSTER CELLS*
Authors:M P Hagan  T Matsushita  T Bonura  A Shotola
Abstract:Abstract— 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.
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