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. A concentration of 3 mM 2-hydroxyethyl methacrylate (HEMA) in a serum free medium was added to ZF4 zebrafish embryo fibroblasts during logarithmic growth and kept on the cells for up to 4 h. Cell death was assayed by the Alamar blue assay 3 days after irradiation. The level of GSH was quantified by a commercial glutathione assay kit. Buthionine sulphoximine (BSO) was used as positive control for depletion of GSH. HEMA reduced the level of GSH relative to control. The cells were irradiated with either broadband UVA (Osram 9W/78), UVB (Philips 9 W PL 12) or 225 keV X-rays. HEMA was non-toxic to the cells under these conditions and did not absorb optical radiation with wavelength longer than 250 nm. Following cell pretreatment with HEMA, the survival relative to controls was reduced from 72.3 % to 23.0 % after exposure to 100 kJ/m^2 of UVA, from 75.3 % to 65.5 % after exposure to 0.25 kJ/m^2 UVB and from 70.0 % to 67.9 % after 16 Gy X-rays. The change in cellular sensitivity due to HEMA was more pronounced with UVA- than with UVB- and X-ray irradiation. UVA-induced cellular damage is characterized by formation of reactive oxygen species, most notably hydrogen peroxide. UVB damage, on the other hand, includes direct interaction with DNA, whereas ionizing radiation induces breaks in the DNA strands, by direct hits or via the formation of hydroxyl radicals. These different mechanisms of action are likely to be associated with the observed sensitivity modifications due to HEMA treatment.