Dental resin monomers induce early and potent oxidative damage on human odontoblast-like cells

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dc.contributor.authorBaldion, Paula Alejandra
dc.contributor.authorVelandia Romero, Myriam L.
dc.contributor.authorCastellanos, Jaime E.
dc.date.accessioned2021-02-26T14:30:43Z
dc.date.available2021-02-26T14:30:43Z
dc.description.abstractenglishResin-based dental materials consist of filler particles and different monomers that are light cured in situ to re-establish dental function and aesthetics. Due to the degree of conversion of adhesive polymers, the monomers triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) are released in relatively high amounts and are susceptible to degradation, acting as bioactive compounds and affecting cell and tissues. This study aimed to assess the effect of HEMA and TEGDMA exposure on metabolic activity, membrane integrity, and cell survival of human odontoblast-like cell (hOLCs). Exposure to resin monomers for 24 h induced major changes in cell membrane integrity, metabolic activity, and survival, which were measured by the calcein method and lactate dehydrogenase release. Increased and early reactive oxygen species (ROS) production was observed leading to degradative oxidation of membrane lipids identified as malondialdehyde production. Severe alteration in mitochondria occurred due to transmembrane mitochondrial potential collapse, possibly inducing activation of apoptotic cell death. hOLCs exposure to resin monomers modified the cell redox potential, with consequences on membrane permeability and integrity, including mitochondrial function. Lipid peroxidation appears to be a key phenomenon for the membrane structures oxidation after HEMA and TEGDMA exposure, leading to cell death and cytotoxicity. hOLCs respond early by differential induction of adaptive mechanisms to maintain cell homeostasis. Modulation of oxidative stress-induced response involves the regulation of genes that encode for antioxidant proteins such as catalase and heme oxygenase-1; regulation that functions as a critical protection mechanism against oxidative cell damage induced by HEMA and TEGDMA. Ascorbic acid as an antioxidant substance mitigates the oxidative damage associated with exposure to monomers.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1016/j.cbi.2020.109336
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.issn1872-7786
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlrepourl:https://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/5453
dc.language.isoeng
dc.publisherElsevier B.V.spa
dc.publisher.journalChemico-Biological Interactionsspa
dc.relation.ispartofseriesChemico-Biological Interactions, 1872-7786, Vol. 333, 2021, p. 109336spa
dc.relation.urihttps://www.sciencedirect.com/science/article/abs/pii/S000927972031557X?via%3Dihub
dc.rights.accessrightshttps://purl.org/coar/access_right/c_abf2
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightsAcceso abierto
dc.rights.creativecommons2021
dc.rights.localAcceso abiertospa
dc.subject.keywordsHydroxyethyl methacrylatespa
dc.subject.keywordsTriethylene glycol dimethacrylatespa
dc.subject.keywordsReactive oxygen speciesspa
dc.subject.keywordsOdontoblastsspa
dc.subject.keywordsCytotoxicityspa
dc.titleDental resin monomers induce early and potent oxidative damage on human odontoblast-like cellsspa
dc.title.translatedDental resin monomers induce early and potent oxidative damage on human odontoblast-like cellsspa
dc.type.coarhttps://purl.org/coar/resource_type/c_6501
dc.type.driverinfo:eu-repo/semantics/article
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.type.localArtículo de revista

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