Lipid Peroxidation as a Possible Cause of Benzoyl Peroxide Toxicity in Rabbit Dental Pulp—A Microsomal Lipid Peroxidation in vitro

Terakado, Masaaki; Yamazaki, Masahito; Tsujimoto, Yasuhisa; Kawashima, Takeshi; Nagashima, Kiichi; Ogawa, Juri; Fujita, Yoshiyuki; Saito, Hiroshi; Sakai, Takeo; Furuyama, Shunsuke

doi:10.1177/00220345840630061801

Cited by 50 publications

(35 citation statements)

References 24 publications

(12 reference statements)

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“…This can be explained by the more hydrophilic character of HEMA, which has an additional hydroxyl group compared with TEGDMA. The higher cytotoxicity of TEGDMA compared with HEMA could further be explained by its ability to interact with the lipid bilayer of cell membranes in a surfactant-like manner 66) and/ or by its ability to cause lipid peroxidation in vitro 67,68) . Both membrane effects can cause cell death 69) .…”

Section: Discussionmentioning

confidence: 99%

NAC ameliorates dental composite-induced DNA double-strand breaks and chromatin condensation

Styllou

Hickel

et al. 2017

Dental Materials Journal

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Released (co)monomers from dental composite components can induce DNA damage of which DNA double-strand breaks (DSBs) threaten genome integrity. Here, we tested whether the administration of the antioxidant N-acetylcysteine (NAC) is able to reduce the dental composite-induced DSBs in primary human gingiva fibroblasts. The dental composites Bis-GMA (bisphenol-Aglycerolate dimethacrylate), GMA (glycidyl methacrylate), HEMA (2-hydroxyethyl methacrylate) and TEGDMA (triethyleneglycol dimethacrylate) were found to induce co-localizing microscopic nuclear foci numbers of the DSB markers γ-H2AX and 53BP1 per cell in the order: GMA>Bis-GMA>TEGDMA>HEMA. Supplementation of (co)monomer-containing culture medium with NAC led to a significant reduction of resin-induced DSBs as well as to an amelioration of dental monomer-induced nuclear chromatin condensation in gingival fibroblasts. Thus, antioxidant treatment can reduce radical-induced chromatin and DNA damage and open avenues to mitigate genotoxic effects of dental composite compounds.

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Section: Discussionmentioning

confidence: 99%

NAC ameliorates dental composite-induced DNA double-strand breaks and chromatin condensation

Styllou

Hickel

et al. 2017

Dental Materials Journal

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“…Interestingly, permanent 3T3 cells were less sensitive to the cytotoxic alterations owing to these two substances in comparison to primary cultures. It was documented by Terakado et al, 30 using the microsomal fraction derived from the rabbit dental pulp, that the initiator DBPO alters biological membranes. This indicates that permanent 3T3 cells are possibly less affected by membrane alterations than the primary cells applied in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, membrane injuries caused by Bis-GMA-induced peroxide formation as well as a high hemolytic activity of Bis-GMA were found. 30,33 Although these bulky and large basic monomers cannot diffuse through the set resin composites and are hardly water-soluble, small amounts of these monomers have been identified in aqueous extracts from polymerized specimens of various resin composites. 2 It may be concluded that these significantly cytotoxic substances should not cause acute damages of the cells.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, the important comonomer TEGDMA may be eluted by water from polymerized composite specimens in quantities significantly exceeding the ED 50 concentrations determined in the present study. 2 In addition, it was documented by various authors 30,34 that TEGDMA may cause microsomal peroxidation and may act on liposomes as a surfactant-like agent solubilizing the lipid bilayer of membranes. Thus, TEGDMA may cause severe pulp alterations if a sufficient cavity lining has not been applied.…”

Section: Discussionmentioning

confidence: 99%

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Cytotoxicity of 35 dental resin composite monomers/additives in permanent 3T3 and three human primary fibroblast cultures

Geurtsen

Lehmann

Spahl³

et al. 1998

J. Biomed. Mater. Res.

452

322

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It was the purpose of this investigation to determine the cytotoxic effects (ED50 concentrations) of 35 monomers or additives identified in commercial dental resin composites. Monolayers of permanent 3T3 cells and three primary human fibroblast types derived from oral tissues (gingiva, pulp, and periodontal ligament) were used as test systems. All substances were tested in concentrations ranging from 0.01 to 5.0 mM. In general, ED50 values varied from 0.06 to > 5 mM. Within the groups of co(monomers), initiators, and cointiators, severe (e.g., Bis-GMA, UDMA, DMBZ, and DMDTA) or moderate (HEMA, BEMA, CQ, DMPT, and DMAPE) cytotoxic effects could be evaluated. Within the group of reaction/decomposition products, only moderate or slight effects were found (ED50: 0.7 to > 5 mM). The inhibitor BHT, the contaminant TPSb, and the photostabilizer HMBP, however, were highly cytotoxic in all cell cultures. In addition, the ED50 values of DBPO and HMBP significantly varied (0.43-3.8 mM, respectively, and 0.44-3.07 mM) with the applied cell culture. Our comprehensive screening shows that for several of the highly cytotoxic composite components, less cytotoxic alternatives are available. Furthermore, there was no cell type identified which was consistently less or more sensitive to the toxic effects of the tested compounds than the others. Primary human periodontal ligament and pulp fibroblasts, however, were found to be more sensitive than 3T3 and gingival fibroblasts to alterations from most tested substances.

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“…It has been reported that TEGDMA can induce lipid peroxidation of microsomes. Furthermore, this comonomer also exhibited surfactant-like potency which may cause detrimental solubilization of the lipid bilayer of cell membranes (Terakado et al, 1984;Fujisawa et al, 1988). Geurtsen et al ( 1998a) investigated cytotoxic effects of 35 single monomers and additives of composite resins in permanent 3T3 cells and three primary human oral fibroblast cultures (Table 1).…”

Section: (G) Pulp Studies In Animals and Humansmentioning

confidence: 99%

Biocompatibility of Resin-Modified Filling Materials

Geurtsen

2000

Critical Reviews in Oral Biology & Medicine

357

258

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Increasing numbers of resin-based dental restorations have been placed over the past decade. During this same period, the public interest in the local and especially systemic adverse effects caused by dental materials has increased significantly It has been found that each resin-based material releases several components into the oral environment. In particular, the comonomer, triethyleneglycol di-methacrylate (TEGDMA), and the 'hydrophilic' monomer, 2-hydroxy-ethyl-methacrylate (HEMA), are leached out from various composite resins and 'adhesive' materials (e.g., resin-modified glass-ionomer cements IGICsl and dentin adhesives) in considerable amounts during the first 24 hours after polymerization. Numerous unbound resin components may leach into saliva during the initial phase after polymerization, and later, due to degradation or erosion of the resinous restoration. Those substances may be systemically distributed and could potentially cause adverse systemic effects in patients. In addition, absorption of organic substances from unpolymerized material, through unprotected skin, due to manual contact may pose a special risk for dental personnel. This is borne out by the increasing numbers of dental nurses, technicians, and aentists who present with allergic reactions to one or more resin components, like HEMA, glutaraldehyde, ethyleneglycol di-methacrylate (EGDMA), and dibenzoyl peroxide (DPO). However, it must be emphasized that, except for conventional composite resins, data reported on the release of substances from resin-based materials are scarce. There is very little reliable information with respect to the biological interactions between resin components and various tissues. Those interactions may be either protective, like absorption to dentin, or detrimental, e.g., inflammatory reactions of soft tissues. Microbial effects have also been observed which may contribute indirectly to caries and irritation of the pulp. Therefore, it is critical, both for our patients and for the profession, that the biological effects of resin-based filling materials be clarified in the near future,

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Lipid Peroxidation as a Possible Cause of Benzoyl Peroxide Toxicity in Rabbit Dental Pulp—A Microsomal Lipid Peroxidation in vitro

Cited by 50 publications

References 24 publications

NAC ameliorates dental composite-induced DNA double-strand breaks and chromatin condensation

NAC ameliorates dental composite-induced DNA double-strand breaks and chromatin condensation

Cytotoxicity of 35 dental resin composite monomers/additives in permanent 3T3 and three human primary fibroblast cultures

Biocompatibility of Resin-Modified Filling Materials

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