HEMA reduced GSH levels and decreased IL-1β release from LPS-stimulated macrophages. The role of GSH in the regulation of IL-1β release was explored. GSH depletion alone could not explain the attenuation of LPS-induced IL-1β release. Electrophile reactivity toward other cellular molecules is a new working hypothesis

Reduction in the amount of glutathione (GSH) in cells can lead to increased sensitivity to physical and chemical agents. Methacrylate monomers (MM) are precursors of polymethacrylates which are used in dental and medical biomaterials and in a wide variety of other products. MM can increase cell sensitivity to long wavelength ultraviolet and visible radiation. The aim of this study is to elucidate if MM can induce sensitivity also to shorter wavelength radiation.

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.

Methacrylate monomers have been identified in aqueous extracts of freshly cured dental fillings. The hypothesis tested presently was that low concentrations of triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) alone or in combination interfere with the LPS-induced release of cytokines from the macrophage cell line RAW264.7.

Induction of cell death by optical radiation in the wavelength range 350–500 nm was significantly increased by commonly used methacrylate monomers, not mediated by absorption of radiation by the methacrylate monomers, but through a mechanism involving rapid reduction in the level of glutathione