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The mechanisms of cytotoxicity of urethane dimethacrylate to Chinese hamster ovary cells

Paper ID Volume ID Publish Year Pages File Format Full-Text
8335 587 2010 9 PDF Available
Title
The mechanisms of cytotoxicity of urethane dimethacrylate to Chinese hamster ovary cells
Abstract

Monomers released from resin-containing products may cause various adverse effects. Urethane dimethacrylate (UDMA) is a principal resin monomer and also a major component released from various dental resin materials. Thus the toxic effects and mechanisms should be elucidated for improving of its safety use. Here we investigated the effects of UDMA on the growth, cell cycle progression, reactive oxygen species (ROS) production and glutathione (GSH) alteration in CHO-K1 cells, and the preventive effects by antioxidants (NAC and catalase) were also evaluated. UDMA elicited growth inhibition (>0.025 mm) of CHO-K1 cells in a clearly dose-dependent manner. Cell cycle perturbation and ROS overproduction were also observed. A 0.1 mm UDMA-induced S-phase cell cycle arrest and ROS accumulation. Cell apoptosis and necrosis became significant when UDMA concentration was 0.25 mm. GSH depletion occurred at cells treated with 0.25 mm UDMA, a highly cytotoxic concentration at which point myriad cells were under apoptosis or necrosis. Thus GSH depletion can be crucial for the death of CHO-K1 cells. Furthermore NAC (0.5–10 mm) and catalase (250–1000 U/ml) obviously attenuated the UDMA-induced toxicity by reducing ROS generation and cell cycle disturbance, and the effects were dose-related. These results suggest that UDMA toxicity is associated with ROS production, GSH depletion, cell cycle disturbance and cell apoptosis/necrosis.

Keywords
Apoptosis; Cell cycle; Cytotoxicity; Glutathione; Reactive oxygen species; Urethane dimethacrylate
First Page Preview
The mechanisms of cytotoxicity of urethane dimethacrylate to Chinese hamster ovary cells
Publisher
Database: Elsevier - ScienceDirect
Journal: Biomaterials - Volume 31, Issue 27, September 2010, Pages 6917–6925
Authors
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Subjects
Physical Sciences and Engineering Chemical Engineering Bioengineering