OBJECTIVES: The photoinitiator camphorquinone (CQ), used in dental restorative materials, was found to be cytotoxic in cell cultures. Previously, we have shown that CQ induces alkali labile sites and DNA strand breaks in human gingival fibroblasts (HGF) associated with an increase of intracellular reactive oxygen species (ROS). Therefore, the objective of our study was to evaluate if DNA damage in HGF cells is caused by the generation of ROS. MATERIAL AND METHODS: HGF cells were treated with different concentrations (0.5-2.5 mM) of CQ. The cell viability was assessed using propidium iodide (PI) assay. Oxidative DNA damage was evaluated by an enzyme-modified comet assay using human 8-hydroxyguanine DNA-glycosylase 1 (hOGG1), which converts oxidized 7,8-dihydro-8-oxoguanine (8-oxoguanine) into DNA strand breaks and functions as a marker for oxidative modified DNA. RESULTS: The results showed that CQ induced DNA damage in HGF cells without cytotoxic effects for the chosen treatment time. CQ treatment led to the generation of 8-oxoguanine in DNA, which can be shown by a significant increase in tail moment after CQ treatment by the enzyme-modified comet assay. CONCLUSION: It may be concluded that DNA damage due to CQ is caused by oxidative stress in gingival fibroblasts. CLINICAL RELEVANCE: A more detailed insight into genotoxic mechanisms in oral cells can be of great importance for a better understanding of the biocompatibility of CQ.
OBJECTIVES: The photoinitiator camphorquinone (CQ), used in dental restorative materials, was found to be cytotoxic in cell cultures. Previously, we have shown that CQ induces alkali labile sites and DNA strand breaks in human gingival fibroblasts (HGF) associated with an increase of intracellular reactive oxygen species (ROS). Therefore, the objective of our study was to evaluate if DNA damage in HGF cells is caused by the generation of ROS. MATERIAL AND METHODS:HGF cells were treated with different concentrations (0.5-2.5 mM) of CQ. The cell viability was assessed using propidium iodide (PI) assay. Oxidative DNA damage was evaluated by an enzyme-modified comet assay using human8-hydroxyguanine DNA-glycosylase 1 (hOGG1), which converts oxidized 7,8-dihydro-8-oxoguanine (8-oxoguanine) into DNA strand breaks and functions as a marker for oxidative modified DNA. RESULTS: The results showed that CQ induced DNA damage in HGF cells without cytotoxic effects for the chosen treatment time. CQ treatment led to the generation of 8-oxoguanine in DNA, which can be shown by a significant increase in tail moment after CQ treatment by the enzyme-modified comet assay. CONCLUSION: It may be concluded that DNA damage due to CQ is caused by oxidative stress in gingival fibroblasts. CLINICAL RELEVANCE: A more detailed insight into genotoxic mechanisms in oral cells can be of great importance for a better understanding of the biocompatibility of CQ.
Authors: Miguel G Neumann; Walter G Miranda; Carla C Schmitt; Frederick A Rueggeberg; Ivo C Correa Journal: J Dent Date: 2005-03-19 Impact factor: 4.379
Authors: Rahul A Datar; Fredrick A Rueggeberg; Gretchen B Caughman; John C Wataha; Jill B Lewis; George S Schuster Journal: J Biomater Sci Polym Ed Date: 2005 Impact factor: 3.517
Authors: Cheryl Lee; Cathal D O'Connell; Carmine Onofrillo; Peter F M Choong; Claudia Di Bella; Serena Duchi Journal: Stem Cells Transl Med Date: 2019-11-26 Impact factor: 6.940