In this study we aimed to further map the suggested relation between GSH-depletion and methacrylate toxicity by comparing the molecular effects of methacrylate exposure and GSH-depletion by inhibiting GSH-synthesis.

The methacrylate monomer 2-hydroxyethyl methacrylate (HEMA) is commonly used in resin-based dental restorative materials. These materials are cured in situ and HEMA and other monomers have been identified in ambient air during dental surgery. In vitro studies have demonstrated a toxic potential of methacrylates, and concerns have been raised regarding possible health effects due to inhalation. In this study we have investigated the mechanisms of HEMA-induced toxicity in the human lung epithelial cell line BEAS-2B..

Methacrylate monomers that are found to leach from cured resin-based dental materials induce biological effects in vitro. The underlying mechanisms have not been fully elucidated although involvement of increased cellular reactive oxygen species (ROS) and DNA-damage has been suggested

Mold spores and their associated mycotoxins have been suggested to be the cause of a variety of human health problems such as asthma and allergic rhinitis related to water-damaged indoor environments. Animal studies have shown that mycotoxins may cause a variety of adverse effects, including acute toxic effects and cancer

Methacrylate monomers have been identified in aqueous extracts of freshly cured compomers. Both cells in the pulpal cavity and various cells of the oral mucosa can potentially be exposed to these leachables.