Stimulation of glutathione depletion, ROS production and cell cycle arrest of dental pulp cells and gingival epithelial cells by HEMA

Chang, Hung‐Hao; Guo, Ming-Kuang; Kasten, Frederick H.; Chang, Mei‐Chi; Huang, Guan‐Tarn; Wang, Yin‐Lin; Wang, Ruey-Song; Jeng, Jiiang‐Huei

doi:10.1016/j.biomaterials.2004.03.021

Cited by 218 publications

(192 citation statements)

References 42 publications

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“…HEMA has a low molecular weight and it has been reported to be more diffusable than monomers which have higher viscosity such as Bis-GMA and UDMA 31) . HEMA induces glutathione depletion and ROS production 32) . ROS production is assumed as an indicator of early oxidative cellular damage induced by resin monomers 4) .…”

Section: Discussionmentioning

confidence: 99%

The protective effect of resveratrol against dentin bonding agents-induced cytotoxicity

et al. 2015

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Bond were added to the medium using extract method. The cells were cultured with or without resveratrol (RES) addition. MTT, reactive oxygen species (ROS), DCF, Comet and 8-OHdG measurements were performed. The agents had a dose-dependent (1:1>1:10>1:20) cytotoxic effect. Considering 1:10 concentration; Group D at 1 h (p<0.01) and Group B and D at 24 h had the weakest cytotoxic effect (p<0.05). After RES addition, the highest cell viability was determined in Groups B+RES and D+RES at 1 h and in Groups A+RES and B+RES at 24 h (p<0.01). The dentin bonding agents induced ROS production and DNA damage regarding to their composition. However, RES addition decreased the indicated parameters.

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Section: Discussionmentioning

confidence: 99%

The protective effect of resveratrol against dentin bonding agents-induced cytotoxicity

et al. 2015

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“…Moreover, HEMA induces morphological changes in cultured cells, such as human pulp fibroblasts (HPFs) and human gingival epithelial cells. HPFs treated with 10 mmol L À1 HEMA presented apparent retraction and loss of filopodia and lamellopodia, the extended cellular processes, which are crucial for cell proliferation and movement during wound healing as well as tissue morphogenesis (Chang et al 2005). HEMA treatment at relatively high concentrations, for example, 5-10 mmol L…”

Section: Hema-induced Apoptosis In Vitromentioning

confidence: 99%

“…They hypothesized that cells differentially activate a balance network of enzymatic cellular antioxidants to control the intracellular oxidative state after exposure to HEMA monomer. It has also been shown that HEMA increases the production of reactive oxygen species, which can cause inflammation (Table 2) and a delay in cell cycle progression (Chang et al 2005, Di Nisio et al 2013. Spagnuolo et al (2004) showed that HEMA-induced ROS production is very important to modulate the activation of nuclear factor kappa B (NF-kB), which plays a protective role to counteract HEMA cytotoxicity.…”

Section: Introductionmentioning

confidence: 99%

HEMA‐induced cytotoxicity: oxidative stress, genotoxicity and apoptosis

2014

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Gallorini M, Cataldi A, di Giacomo V. HEMA-induced cytotoxicity: oxidative stress, genotoxicity and apoptosis.International Endodontic Journal, 47, 813-818, 2014. Dental resin composites consist of organic polymers with inorganic fillers used as bonding resins and direct filling materials in dentine adhesives and as sealing agents for inlays, crowns and orthodontic brackets. Despite various modifications in the formulation, the chemical composition of composite resins includes inorganic filler particles and additives, which are incorporated into a mixture of an organic resin matrix. Among them, 2-hydroxyethylmethacrylate (HEMA) is one of the most frequently used. Several studies have attempted to clarify the mechanisms underlying HEMA cytotoxicity. Most of them support the hypothesis that this compound, once released in the oral environment, increases reactive oxygen species (ROS) production and oxidative DNA damage through double-strand breaks evidenced by in vitro presence of micronuclei. As a consequence, the glutathione detoxifying intracellular pool forms adducts with HEMA through its cysteine motif and inflammation begins to occur: transcription of early genes of inflammation such as tumour necrosis factor a or inducible cyclooxygenase up to the secretion of prostaglandins 2. These phenomena are counteracted by N-acetylcysteine (NAC), a nonenzymatic antioxidant, but not by vitamin E or other antioxidant. Consequently, NAC prevents HEMA-induced apoptosis acting as a direct ROS scavenger. This minireview collects the most significant papers on HEMA and tries to make an overview of its cytotoxicity on different cell types and experimental models.

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“…Resin monomers such as triethyleneglycol dimethacrylate and 2-hydroxyethyl methacrylate have been found to deplete glutathione and induce cellular oxidative stress, resulting in cytotoxicity 15,16) . Resinbased dentine bonding agents were also found to reduce intracellular glutathione 17) .…”

Section: Discussionmentioning

confidence: 99%

The effects of restorative composite resins on the cytotoxicity of dentine bonding agents

et al. 2013

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During restoration of damaged teeth in dental clinics, dentin bonding agents are usually overlaid with restorative resin composites. The purpose of this study was to investigate the effects of restorative resin composites on cytotoxicity of dentin bonding agents. Dentin bonding agents were placed on glass discs, pre-cured and uncured resin composite discs. Bonding agents on the glass discs and composite resins discs were light cured and used for agar overlay cytotoxicity testing. Dentin bonding agents on composite resin discs exhibited far less cytotoxicity than that on glass discs. The polymerization of resin composite increased the surface hardness and decreased the cytotoxicity of bonding agents. In conclusion, composite resins in dental restorations are expected to enhance the polymerization of dentin bonding agents and reduce the elution of resin monomers, resulting in the decrease of cytotoxicity.

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Stimulation of glutathione depletion, ROS production and cell cycle arrest of dental pulp cells and gingival epithelial cells by HEMA

Cited by 218 publications

References 42 publications

The protective effect of resveratrol against dentin bonding agents-induced cytotoxicity

The protective effect of resveratrol against dentin bonding agents-induced cytotoxicity

HEMA‐induced cytotoxicity: oxidative stress, genotoxicity and apoptosis

The effects of restorative composite resins on the cytotoxicity of dentine bonding agents

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