A subsequent induction of base excision repair inhibits rejoining of nucleotide excision repair

• Main Authors: Pei-Yi, 李姵儀
• Other Authors: Yin-Chang Liu
• Format: Others
• Language: en_US
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/50045450334638134780

碩士 === 中山醫學大學 === 生化暨生物科技研究所 === 96 === DNA damage can be caused by exposure to environmental agents or by normal cellular metabolic processes that can cause cell killing, mutation, tumorigenesis, cell cycle arrest, neoplasm transformation, and activation of DNA repair. Recent study indicates that the drug may have potential to interact with DNA and cause DNA damage in human cells. Amoxicillin is a commonly prescribed drug for anti- bacterial infection. In this study, we are interested in the effect of the drug on the cellular DNA integrity. Amoxicillin was added to the human cells in culture, and the DNA adducts induced by the drug were accessed by a comet-NE assay. The results show the intracellular reactive oxygen species (ROS) were increased after amoxicillin treatment. Thus, we suggest that amoxicillin causes oxidative DNA damage in mammalian cells via ROS. Otherwise, we have noted that colcemid or amoxicillin, when they were present in cells recovering from UV irradiation, the gap-rejoining during the NER was perturbed. The similar effect on rejoining were also found when cells treatment with taxol or MMS. We suspected that an induction oxidative DNA damages immediately following UV irradiation would perturb the rejoining of NER as the result of competition between NER and BER for rejoining the gaps produced during the repair process. Thus, we hypothesize that an induction subsequent to NER could jeopardize the completion of NER.