| Budget Amount *help |
¥9,300,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2005: ¥5,900,000 (Direct Cost: ¥5,900,000)
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| Research Abstract |
The effects of HEMA and TEGDMA, thecomponents of dentin bonding agents, on HSE transactivation were investigated with reporter assay in THP-1 human monocytic cells. The results showed HEMA inhibited the HSE transactivation depending on the concentration of HEMA. TEGDMA, however, did not inhibit the HSE transactivation. HEMA and TEGDMA are known to inhibit HSP70 induction. Therefore, the results in the present research suggested that there is the difference between HEMA and TEGDMA in the mechanism of the inhibition to induce HSP70.
Dentin bonding agents have incomplete polymerization of these monomers and their leaching into adjacent (pulpal) oral tissues has raised concerns about their biocompatibility. The sublethal effects of these resins are virtually unknown, but their electrophilic nature led to the hypothesis that they may alter cellular oxidative stress pathways. Glutathione balance between reduced (GSH) and oxidized (GSSG) is a major mechanism by which cells maintain redox balan
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ce and was therefore the focus of the current investigation. THP-1 human monocytic cells were exposed to HEMA, BPO, CQ, or TEGDMA for 24 h at sublethal doses, then GSH and GSSG levels were measured by means of Ellman's method adapted for cell culture. The results indicate that these dental resin compounds act at least partly via oxidative stress by increasing GSH levels at sublethal concentrations. However, the GSH-GSSG ratio was relatively unaffected. Only BPO altered the GSH-GSSG ratio at 24 h, again at sublethal levels (7.5-15_mol/L). The results support the hypothesis that resin monomers act, at least in part, via oxidative stress, and that oxidative-stress pathways should be one focus of future investigations of monomer biocompatibility.
Resin composites in dentistry are polymerized in situ using a blue-light activated, free-radical polymerization mechanism. Blue light (400-500 nm) is used to activate camphoroquinone (CQ), which decomposes to form free radicals that are stabilized by dimethyl-p-toludine (DMPT). CQ and DMPT are applied near tooth pulpal tissues and are irradiated during restorative procedures. Because glutathione is a major component of the cellular redox management system, we tested the hypothesis that blue light irradiation would shift cellular glutathione redox balance of cells exposed to CQ and DMPT. We also measured NF-kB activation, a redox-sensitive transcription factor that regulates inflammatory responses and glutathione synthetic enzyme levels. THP1 human monocytes were exposed to sublethal levels of CQ (0.4 mM) or DMPT (1.0 mM), with or without blue light exposure (25 J/cm2) from a quartz-tungsten-halogen source. The ratio of reduced to oxidized glutathione was measured using as assay based on 5,50-dithio-bis (2-nitrobenszoic acid). NFjB transactivation was measured by transfection of an NF-kB-containing plasmid linked to a luciferase reporter. Our results showed that blue light, CQ, or DMPT alone had no significant effect cellular glutathione redox balance, but that the combination of these agents induced a marked oxidative bias, and reduced total glutathione levels up to 50%. On the other hand light, CQ and DMPT alone or in combination suppressed NF-kB transactivation by >70%. Our results suggest that CQ and DMPT pose risks to pulpal tissues with or without blue light irradiation, and that multiple, interacting mechanisms shape the response to these agents. Less
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