Radicals produced by blue-light–resin interactions alter the redox status of THP1 human monocytes
✍ Scribed by M. Noda; J.C. Wataha; H. Kachi; J.B. Lewis; R.L. Messer; H. Sano
- Book ID
- 102295037
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 291 KB
- Volume
- 83A
- Category
- Article
- ISSN
- 1549-3296
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✦ Synopsis
Abstract
Resin composites are widely used in dentistry, and are polymerized in situ using a blue‐light activated, free‐radical polymerization mechanism. Blue light (400–500nm) 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, suggesting that pulpal cells are exposed to free radicals. 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 NFκB 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 m__M__) or DMPT (1.0 m__M__), with or without blue light exposure (25 J/cm^2^) from a quartz‐tungsten‐halogen source. The ratio of reduced to oxidized glutathione was measured using as assay based on 5,5′‐dithio‐bis(2‐nitrobenszoic acid). NFκB transactivation was measured by transfection of an NFκB‐containing plasmid linked to a luciferase reporter. Our results showed that blue light, CQ, or DMPT alone had no significant effect on 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 NFκB 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. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res 2007