Cell toxicity of methacrylate monomers-The role of glutathione adduct formation
Polymer‐based dental restorative materials are designed to polymerize in situ. However, the conversion of methacrylate monomer to polymer is never complete, and leakage of the monomer occurs. It has been shown that these monomers are toxic in vitro; hence concerns regarding exposure of patients and...
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| Veröffentlicht in: | Journal of biomedical materials research. Part A 2013-12, Vol.101 (12), p.3504-3510 |
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| creator | Ansteinsson, V. Kopperud, H. B. Morisbak, E. Samuelsen, J. T. |
| description | Polymer‐based dental restorative materials are designed to polymerize in situ. However, the conversion of methacrylate monomer to polymer is never complete, and leakage of the monomer occurs. It has been shown that these monomers are toxic in vitro; hence concerns regarding exposure of patients and dental personnel have been raised. Different monomer methacrylates are thought to cause toxicity through similar mechanisms, and the sequestration of cellular glutathione (GSH) may be a key event. In this study we examined the commonly used monomer methacrylates, 2‐hydroxyethylmethacrylate (HEMA), triethylenglycol‐dimethacrylate (TEGDMA), bisphenol‐A‐glycidyl‐dimethacrylate (BisGMA), glycerol‐dimethacrylate (GDMA) and methyl‐methacrylate (MMA). The study aimed to establish monomers' ability to complex with GSH, and relate this to cellular toxicity endpoints. Except for BisGMA, all the monomer methacrylates decreased the GSH levels both in cells and in a cell‐free system. The spontaneous formation of methacrylate‐GSH adducts were observed for all methacrylate monomers except BisGMA. However, we were not able to correlate GSH depletion and toxic response measured as SDH activity and changes in cell growth pattern. Together, the current study indicates mechanisms other than GSH‐binding to be involved in the toxicity of methacrylate monomers. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 101A: 3504–3510, 2013. |
| doi_str_mv | 10.1002/jbm.a.34652 |
| format | Article |
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B. ; Morisbak, E. ; Samuelsen, J. T.</creator><creatorcontrib>Ansteinsson, V. ; Kopperud, H. B. ; Morisbak, E. ; Samuelsen, J. T.</creatorcontrib><description>Polymer‐based dental restorative materials are designed to polymerize in situ. However, the conversion of methacrylate monomer to polymer is never complete, and leakage of the monomer occurs. It has been shown that these monomers are toxic in vitro; hence concerns regarding exposure of patients and dental personnel have been raised. Different monomer methacrylates are thought to cause toxicity through similar mechanisms, and the sequestration of cellular glutathione (GSH) may be a key event. In this study we examined the commonly used monomer methacrylates, 2‐hydroxyethylmethacrylate (HEMA), triethylenglycol‐dimethacrylate (TEGDMA), bisphenol‐A‐glycidyl‐dimethacrylate (BisGMA), glycerol‐dimethacrylate (GDMA) and methyl‐methacrylate (MMA). The study aimed to establish monomers' ability to complex with GSH, and relate this to cellular toxicity endpoints. Except for BisGMA, all the monomer methacrylates decreased the GSH levels both in cells and in a cell‐free system. The spontaneous formation of methacrylate‐GSH adducts were observed for all methacrylate monomers except BisGMA. However, we were not able to correlate GSH depletion and toxic response measured as SDH activity and changes in cell growth pattern. Together, the current study indicates mechanisms other than GSH‐binding to be involved in the toxicity of methacrylate monomers. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 101A: 3504–3510, 2013.</description><identifier>ISSN: 1549-3296</identifier><identifier>EISSN: 1552-4965</identifier><identifier>DOI: 10.1002/jbm.a.34652</identifier><identifier>PMID: 23613115</identifier><language>eng</language><publisher>Hoboken, NJ: Blackwell Publishing Ltd</publisher><subject>Biological and medical sciences ; Cell Cycle - drug effects ; Cell Line ; Cell-Free System ; dental restorative materials ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Glutathione - metabolism ; GSH ; Head and neck surgery. Maxillofacial surgery. Dental surgery. Orthodontics ; Humans ; Mass Spectrometry ; Maxillofacial surgery. Dental surgery. Orthodontics ; Medical sciences ; methacrylate monomers ; Methacrylates - chemistry ; Methacrylates - toxicity ; oxidative stress ; Polymers - chemistry ; Polymers - toxicity ; Succinate Dehydrogenase - metabolism ; Surgery (general aspects). 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B.</creatorcontrib><creatorcontrib>Morisbak, E.</creatorcontrib><creatorcontrib>Samuelsen, J. T.</creatorcontrib><title>Cell toxicity of methacrylate monomers-The role of glutathione adduct formation</title><title>Journal of biomedical materials research. Part A</title><addtitle>J. Biomed. Mater. Res</addtitle><description>Polymer‐based dental restorative materials are designed to polymerize in situ. However, the conversion of methacrylate monomer to polymer is never complete, and leakage of the monomer occurs. It has been shown that these monomers are toxic in vitro; hence concerns regarding exposure of patients and dental personnel have been raised. Different monomer methacrylates are thought to cause toxicity through similar mechanisms, and the sequestration of cellular glutathione (GSH) may be a key event. In this study we examined the commonly used monomer methacrylates, 2‐hydroxyethylmethacrylate (HEMA), triethylenglycol‐dimethacrylate (TEGDMA), bisphenol‐A‐glycidyl‐dimethacrylate (BisGMA), glycerol‐dimethacrylate (GDMA) and methyl‐methacrylate (MMA). The study aimed to establish monomers' ability to complex with GSH, and relate this to cellular toxicity endpoints. Except for BisGMA, all the monomer methacrylates decreased the GSH levels both in cells and in a cell‐free system. The spontaneous formation of methacrylate‐GSH adducts were observed for all methacrylate monomers except BisGMA. However, we were not able to correlate GSH depletion and toxic response measured as SDH activity and changes in cell growth pattern. Together, the current study indicates mechanisms other than GSH‐binding to be involved in the toxicity of methacrylate monomers. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 101A: 3504–3510, 2013.</description><subject>Biological and medical sciences</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Line</subject><subject>Cell-Free System</subject><subject>dental restorative materials</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Glutathione - metabolism</subject><subject>GSH</subject><subject>Head and neck surgery. Maxillofacial surgery. Dental surgery. Orthodontics</subject><subject>Humans</subject><subject>Mass Spectrometry</subject><subject>Maxillofacial surgery. Dental surgery. Orthodontics</subject><subject>Medical sciences</subject><subject>methacrylate monomers</subject><subject>Methacrylates - chemistry</subject><subject>Methacrylates - toxicity</subject><subject>oxidative stress</subject><subject>Polymers - chemistry</subject><subject>Polymers - toxicity</subject><subject>Succinate Dehydrogenase - metabolism</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Technology. Biomaterials. Equipments</subject><subject>toxicity</subject><issn>1549-3296</issn><issn>1552-4965</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90E1P3DAQBmALUZWvnnqvckFCqrL1d-IjrFqg2oJUUcHNcpwxG0jWYDsq--_xsgvcONmyn5mxX4S-EjwhGNMfd80wMRPGpaBbaJcIQUuupNhe7bkqGVVyB-3FeJexxIJ-RjuUScIIEbvocgp9XyT_1NkuLQvvigHS3Niw7E2CYvALP0CI5dUciuB7WInbfkwmzTu_gMK07WhT4XwYTMonB-iTM32EL5t1H_379fNqelbOLk_Pp8ez0nKlaFnXyllmpZW0kU5VTQvSSEJrxy00BNeMOQK4UsY1grUVlQo3NeaEinycr_fR0brvQ_CPI8Skhy7a_BezAD9GTXglhGAS00y_r6kNPsYATj-EbjBhqQnWqwR1TlAb_ZJg1t82jcdmgPbNvkaWweEGmGhN74JZ2C6-u0pxRunqhXTt_nc9LD-aqX-f_Dl-nV6ui7qY4OmtyIR7LStWCX19capPzm747PrvVAv2DDhHl8A</recordid><startdate>201312</startdate><enddate>201312</enddate><creator>Ansteinsson, V.</creator><creator>Kopperud, H. B.</creator><creator>Morisbak, E.</creator><creator>Samuelsen, J. T.</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201312</creationdate><title>Cell toxicity of methacrylate monomers-The role of glutathione adduct formation</title><author>Ansteinsson, V. ; Kopperud, H. B. ; Morisbak, E. ; Samuelsen, J. T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4992-889fc3c6c62b6f97bde6a6128f4ceb10833f1e079afb53d72690b8041251e0083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Biological and medical sciences</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Line</topic><topic>Cell-Free System</topic><topic>dental restorative materials</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Glutathione - metabolism</topic><topic>GSH</topic><topic>Head and neck surgery. Maxillofacial surgery. Dental surgery. Orthodontics</topic><topic>Humans</topic><topic>Mass Spectrometry</topic><topic>Maxillofacial surgery. Dental surgery. Orthodontics</topic><topic>Medical sciences</topic><topic>methacrylate monomers</topic><topic>Methacrylates - chemistry</topic><topic>Methacrylates - toxicity</topic><topic>oxidative stress</topic><topic>Polymers - chemistry</topic><topic>Polymers - toxicity</topic><topic>Succinate Dehydrogenase - metabolism</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Technology. Biomaterials. Equipments</topic><topic>toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ansteinsson, V.</creatorcontrib><creatorcontrib>Kopperud, H. B.</creatorcontrib><creatorcontrib>Morisbak, E.</creatorcontrib><creatorcontrib>Samuelsen, J. 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T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cell toxicity of methacrylate monomers-The role of glutathione adduct formation</atitle><jtitle>Journal of biomedical materials research. Part A</jtitle><addtitle>J. Biomed. Mater. Res</addtitle><date>2013-12</date><risdate>2013</risdate><volume>101</volume><issue>12</issue><spage>3504</spage><epage>3510</epage><pages>3504-3510</pages><issn>1549-3296</issn><eissn>1552-4965</eissn><abstract>Polymer‐based dental restorative materials are designed to polymerize in situ. However, the conversion of methacrylate monomer to polymer is never complete, and leakage of the monomer occurs. It has been shown that these monomers are toxic in vitro; hence concerns regarding exposure of patients and dental personnel have been raised. Different monomer methacrylates are thought to cause toxicity through similar mechanisms, and the sequestration of cellular glutathione (GSH) may be a key event. In this study we examined the commonly used monomer methacrylates, 2‐hydroxyethylmethacrylate (HEMA), triethylenglycol‐dimethacrylate (TEGDMA), bisphenol‐A‐glycidyl‐dimethacrylate (BisGMA), glycerol‐dimethacrylate (GDMA) and methyl‐methacrylate (MMA). The study aimed to establish monomers' ability to complex with GSH, and relate this to cellular toxicity endpoints. Except for BisGMA, all the monomer methacrylates decreased the GSH levels both in cells and in a cell‐free system. The spontaneous formation of methacrylate‐GSH adducts were observed for all methacrylate monomers except BisGMA. However, we were not able to correlate GSH depletion and toxic response measured as SDH activity and changes in cell growth pattern. Together, the current study indicates mechanisms other than GSH‐binding to be involved in the toxicity of methacrylate monomers. © 2013 Wiley Periodicals, Inc. 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| subjects | Biological and medical sciences Cell Cycle - drug effects Cell Line Cell-Free System dental restorative materials Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - metabolism Glutathione - metabolism GSH Head and neck surgery. Maxillofacial surgery. Dental surgery. Orthodontics Humans Mass Spectrometry Maxillofacial surgery. Dental surgery. Orthodontics Medical sciences methacrylate monomers Methacrylates - chemistry Methacrylates - toxicity oxidative stress Polymers - chemistry Polymers - toxicity Succinate Dehydrogenase - metabolism Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Technology. Biomaterials. Equipments toxicity |
| title | Cell toxicity of methacrylate monomers-The role of glutathione adduct formation |
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