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首页> 外文期刊>Journal of biomedical materials research. Part B, Applied biomaterials. >Effects of the iron-chelating agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity.
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Effects of the iron-chelating agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity.

机译：铁螯合剂去铁胺对三甘醇二甲基丙烯酸酯，甲基丙烯酸2-羟乙酯，过氧化氢诱导的细胞毒性的影响。

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摘要

Triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxylethyl methacrylate (HEMA) are known to deplete glutathione in mammalian cells, generate reactive oxygen species (ROS), and cause oxidative stress. In this study, we investigated whether hydroxyl radicals (.OH), the most lethal and genotoxic ROS, and the Fenton reaction are involved in the cytotoxicity of resin monomers to four different cell types, namely MC3T3-E1 preosteoblasts, human dental pulp cells (HDPCs), human gingival fibroblasts, and L929 mouse fibroblasts. Deferoxamine (DFO), an iron chelating agent, effectively protected MC3T3-E1 cells from resin monomer-induced cytotoxicity, indicating that cytotoxicity was caused primarily by hydroxyl radicals. However, DFO only had a protective effect against relatively high concentrations of TEGDMA and HEMA in HDPCs and human gingival fibroblasts, and resin monomer-induced cytotoxicity in L929 was not attenuated by DFO. A labile iron pool (LIP) was detectable only in MC3T3-E1 cells among the four cell types. This indicates that the generation of hydroxyl radicals induced by resin monomers is likely dependent on LIP levels. In contrast to resin monomers, hydrogen peroxide (H(2)O(2))-induced cytotoxicity was not prevented by DFO in any of the cell types examined, although hydroxyl radicals were detected in MC3T3-E1 cells and HDPCs on exposure to exogenous H(2)O(2). This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H(2)O(2)-treated cells.
机译：已知三甘醇二甲基丙烯酸酯（TEGDMA）和甲基丙烯酸2-羟乙酯（HEMA）会耗尽哺乳动物细胞中的谷胱甘肽，产生活性氧（ROS）并引起氧化应激。在这项研究中，我们调查了羟基自由基（.OH），最具致死性和遗传毒性的ROS和Fenton反应是否与树脂单体对四种不同细胞类型的细胞毒性有关，这些细胞类型包括MC3T3-E1前成骨细胞，人牙髓细胞（ HDPC），人牙龈成纤维细胞和L929小鼠成纤维细胞。铁螯合剂去铁胺（DFO）有效保护MC3T3-E1细胞免受树脂单体诱导的细胞毒性作用，表明细胞毒性主要由羟基自由基引起。但是，DFO仅对HDPC和人牙龈成纤维细胞中相对较高的TEGDMA和HEMA浓度具有保护作用，并且DFO不会减弱L929中树脂单体诱导的细胞毒性。仅在四种细胞类型中的MC3T3-E1细胞中可检测到不稳定的铁池（LIP）。这表明由树脂单体诱导的羟基自由基的产生可能取决于LIP水平。与树脂单体相反，尽管在暴露于外源的MC3T3-E1细胞和HDPCs中检测到羟基自由基，但在任何检测的细胞类型中DFO均不能阻止过氧化氢（H（2）O（2））诱导的细胞毒性。 H（2）O（2）。此结果表明，羟基自由基的产生并不总是H（2）O（2）处理细胞中细胞毒性的主要原因。

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