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Illuminating the cellular and molecular mechanism of the potential toxicity of methacrylate monomers used in biomaterials
J. Juráňová,
Language English Country United States
Document type Journal Article, Review
- MeSH
- Acetylcysteine pharmacology MeSH
- Biocompatible Materials chemistry toxicity MeSH
- Glutathione metabolism MeSH
- Polymethacrylic Acids chemistry toxicity MeSH
- Humans MeSH
- Methacrylates chemistry toxicity MeSH
- Polyethylene Glycols chemistry toxicity MeSH
- Reactive Oxygen Species metabolism MeSH
- Free Radical Scavengers pharmacology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
The cytotoxicity of methacrylate-based biopolymers crosslinked by in situ photopolymerization has been attributed mainly to residual methacrylate monomers released due to incomplete polymerization. The residual monomers, primarily triethyleneglycol dimethacrylate or 2-hydroxyethyl methacrylate, may irritate adjacent tissue, or be released into the bloodstream and reach practically all tissues. Increased production of reactive oxygen species, which may be connected to concomitant glutathione depletion, has been the most noticeable effect observed in vitro following the exposure of cells to methacrylates. Radical scavengers such as glutathione or N-acetylcysteine represent the most important cellular strategy against methacrylate-induced toxicity by direct adduct formation, resulting in monomer detoxification. Reactive oxygen species may participate in methacrylate-induced genotoxic or pro-apoptotic effects and cell-cycle arrest via induction of corresponding molecular pathways in cells. A deeper understanding of the biological mechanisms and effects of methacrylates widely used in various bioapplications may enable a better estimation of potential risks and thus, selection of a more appropriate composition of polymer material to eliminate potentially harmful substances such as triethyleneglycol dimethacrylate.
References provided by Crossref.org
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- $a Juráňová, Jana $u Department of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacky University, Hněvotínská 3, Olomouc, Czech Republic. Faculty of Medicine and Dentistry, Institute of Molecular and Translational Medicine, Palacky University, Hněvotínská 5, Olomouc, Czech Republic.
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- $a The cytotoxicity of methacrylate-based biopolymers crosslinked by in situ photopolymerization has been attributed mainly to residual methacrylate monomers released due to incomplete polymerization. The residual monomers, primarily triethyleneglycol dimethacrylate or 2-hydroxyethyl methacrylate, may irritate adjacent tissue, or be released into the bloodstream and reach practically all tissues. Increased production of reactive oxygen species, which may be connected to concomitant glutathione depletion, has been the most noticeable effect observed in vitro following the exposure of cells to methacrylates. Radical scavengers such as glutathione or N-acetylcysteine represent the most important cellular strategy against methacrylate-induced toxicity by direct adduct formation, resulting in monomer detoxification. Reactive oxygen species may participate in methacrylate-induced genotoxic or pro-apoptotic effects and cell-cycle arrest via induction of corresponding molecular pathways in cells. A deeper understanding of the biological mechanisms and effects of methacrylates widely used in various bioapplications may enable a better estimation of potential risks and thus, selection of a more appropriate composition of polymer material to eliminate potentially harmful substances such as triethyleneglycol dimethacrylate.
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