Effects of the iron-chelating agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity

Authors

  • Tingting Zhu,

    1. Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University, Chongro-ku, Seoul 110-749, Korea
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    • Both authors contributed equally to this work.

  • Bum-Soon Lim,

    1. Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University, Chongro-ku, Seoul 110-749, Korea
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    • Both authors contributed equally to this work.

  • Hee Chul Park,

    1. Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University, Chongro-ku, Seoul 110-749, Korea
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  • Kyung Mi Son,

    1. Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University, Chongro-ku, Seoul 110-749, Korea
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  • Hyeong-Cheol Yang

    Corresponding author
    1. Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University, Chongro-ku, Seoul 110-749, Korea
    • Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University, Chongro-ku, Seoul 110-749, Korea
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  • How to cite this article: Zhu T, Lim B-S, Park HC, Son KM, Yang H-C. 2012. Effects of the iron-chelating agent deferoxamine on triethylene glycol dimethacrylate, 2-hydroxylethyl methacrylate, hydrogen peroxide-induced cytotoxicity. J Biomed Mater Res Part B 2012:100B:197-205.

Abstract

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 (H2O2)-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 H2O2. This result suggests that generation of hydroxyl radicals is not always the primary cause of cytotoxicity in H2O2-treated cells. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2012.

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