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• W2047761750 endingPage "818" @default.
• W2047761750 startingPage "813" @default.
• W2047761750 abstract "Abstract Dental resin composites consist of organic polymers with inorganic fillers used as bonding resins and direct filling materials in dentine adhesives and as sealing agents for inlays, crowns and orthodontic brackets. Despite various modifications in the formulation, the chemical composition of composite resins includes inorganic filler particles and additives, which are incorporated into a mixture of an organic resin matrix. Among them, 2‐hydroxyethylmethacrylate (HEMA) is one of the most frequently used. Several studies have attempted to clarify the mechanisms underlying HEMA cytotoxicity. Most of them support the hypothesis that this compound, once released in the oral environment, increases reactive oxygen species (ROS) production and oxidative DNA damage through double‐strand breaks evidenced by in vitro presence of micronuclei. As a consequence, the glutathione detoxifying intracellular pool forms adducts with HEMA through its cysteine motif and inflammation begins to occur: transcription of early genes of inflammation such as tumour necrosis factor α or inducible cyclooxygenase up to the secretion of prostaglandins 2. These phenomena are counteracted by N‐acetylcysteine (NAC), a nonenzymatic antioxidant, but not by vitamin E or other antioxidant. Consequently, NAC prevents HEMA‐induced apoptosis acting as a direct ROS scavenger. This minireview collects the most significant papers on HEMA and tries to make an overview of its cytotoxicity on different cell types and experimental models." @default.
• W2047761750 created "2016-06-24" @default.
• W2047761750 creator A5055320904 @default.
• W2047761750 creator A5055796767 @default.
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• W2047761750 date "2014-01-28" @default.
• W2047761750 modified "2023-10-11" @default.
• W2047761750 title "HEMA-induced cytotoxicity: oxidative stress, genotoxicity and apoptosis" @default.
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• W2047761750 doi "https://doi.org/10.1111/iej.12232" @default.
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