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Figure 1. Model of the induction of genotoxicity in mammalian cells by triethylene glycol dimethacrylate (TEGDMA) and cellular responses. DNA damage by TEGDMA may occur either directly, via covalent binding to nucleophilic centers of double-stranded DNA, or indirectly, via the generation of reactive oxygen species (ROS). The replication of damaged DNA causes gene mutations, but the successful repair of damaged DNA will lead to cell survival. Incomplete repair, however, as well as DNA double-strand breaks (dsb) as a result of blocked DNA replication, will cause cell-cycle delay or apoptosis in the case of severe and irreversible damage. Genotoxicity and cell-cycle delay are inhibited in the presence of the ROS scavenger N-acetylcysteine (NAC).
J DENT RES, Vol. 85, No. 10,
870-877 (2006)
DOI: 10.1177/154405910608501001
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