Cell toxicity of HEMA – the role of oxidative stress
The methacrylate monomer 2-hydroxyethyl methacrylate (HEMA) is commonly used in polymer-based dental restorative materials. Several studies have shown that HEMA is toxic in vitro. Increased oxidative stress has been suggested as a key event in this response.
Objective: To study the relation between decreased viability in human bronchial epithelial cells exposed to HEMA and oxidative stress.
Method: Cells of the human bronchial epithelial cell line BEAS 2B were exposed to HEMA (1.25–5 mM) for up to 96 hours. Cell viability was estimated using the MTT method and fluorescence microscopy. Levels of glutathione (GSH), reactive oxygen species (ROS) and cell cycle analysis were determined by flow cytometry. The cells were incubated with L-buthionine sulfoximine (BSO) to inhibit glutathione synthesis and compared to the effects of HEMA exposure, and exposed to HEMA in the presence of an antioxidant (vitamin C).
Result: Reduced cell proliferation and increased apoptosis were observed in BEAS 2B cells after 24 hours of HEMA exposure. This was preceded by depletion of cellular GSH and increased levels of ROS. BSO incubation resulted in a similar GSH depletion and ROS increase, but did not alter the cell proliferation or induce cell death. Vitamin C attenuated the HEMA-induced ROS formation without inhibiting cell death or altering cell proliferation.
Conclusion: HEMA reduced cell proliferation and increased apoptosis in human lung epithelial cells. Our results show that this is not solely caused by oxidative stress.
