Schweikl H, Hartmann A, Hiller K-A, Spagnuolo G, Bolay C, Brockhoff G, Schmalz G
Department of Operative Dentistry and Periodontology, University of Regensburg, D-93042 Regensburg, Germany.
Dent Mater. 2007 Jun;23(6):688-95. doi: 10.1016/j.dental.2006.06.021. Epub 2006 Aug 7.
Dental resin monomers like triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) are able to cause an imbalance of the redox state in mammalian cells. The resulting oxidative stress originating from reactive oxygen species (ROS) has been associated with cytotoxicity. We hypothesized that ROS might contribute to the generation of genotoxicity by TEGDMA and HEMA as well. Therefore, we examined the formation of micronuclei in V79 cells by both resin monomers in the presence of the antioxidant N-acetylcysteine (NAC), which scavenges ROS. In addition, we analyzed the effects of TEGDMA and HEMA on the normal cell cycle in the presence of NAC.
V79 fibroblasts were exposed to increasing concentrations of TEGDMA and HEMA in the presence and absence of NAC for 24h. Genotoxicity was indicated by the formation of micronuclei. The modification of the normal cell cycle was analyzed by flow cytometry (FACS).
A dose-related increase in the number of micronuclei in V79 cells-induced by TEGDMA and HEMA indicated genotoxicity of both chemicals. However, the formation of micronuclei was reduced in the presence of 10 mmol/L NAC, indicating its protective role. A cell cycle delay in G2 phase caused by TEGDMA was absent when cells were co-treated with NAC. Similarly, the presence of NAC led to a reversion of the cell cycle delay in HEMA-treated cell cultures.
Our results suggest that genotoxic effects and the modification of the cell cycle caused by TEGDMA and HEMA are mediated, at least in part, by oxidative stress.
牙科树脂单体如二缩三乙二醇二甲基丙烯酸酯（TEGDMA）和甲基丙烯酸2-羟乙酯（HEMA）能够导致哺乳动物细胞氧化还原状态失衡。活性氧（ROS）产生的氧化应激与细胞毒性有关。我们推测ROS可能也有助于TEGDMA和HEMA产生遗传毒性。因此，我们在抗氧化剂N-乙酰半胱氨酸（NAC）存在的情况下，研究了这两种树脂单体在V79细胞中微核的形成，NAC可清除ROS。此外，我们分析了在NAC存在的情况下TEGDMA和HEMA对正常细胞周期的影响。
将V79成纤维细胞在有或无NAC的情况下，暴露于浓度不断增加的TEGDMA和HEMA中24小时。微核的形成表明遗传毒性。通过流式细胞术（FACS）分析正常细胞周期的改变。
TEGDMA和HEMA诱导的V79细胞中微核数量呈剂量相关增加，表明这两种化学物质具有遗传毒性。然而，在10 mmol/L NAC存在的情况下，微核的形成减少，表明其具有保护作用。当细胞与NAC共同处理时，TEGDMA引起的G2期细胞周期延迟消失。同样，NAC的存在导致HEMA处理的细胞培养物中细胞周期延迟的逆转。
我们的结果表明，TEGDMA和HEMA引起的遗传毒性作用和细胞周期改变至少部分是由氧化应激介导的。
