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Combined effects of 2-hydroxyethyl methacrylate and nicotine in THP-1 cells

Resin-based dental restorative materials are in widespread use. The resin is usually made up from methacrylate monomers that are polymerized in situ. This process is never complete and monomer leakage from set materials causes exposure of the dental patient. Most studies addressing toxicity of chemicals, including methacrylates, investigate the chemical alone in different in vitro systems. Individuals are, however, normally exposed to an ill-defined combination of environmental chemicals. The effects of such combined exposure may differ considerably from the effect of each compound.

Objective: Simultaneous exposure to nicotine and 2-hydroxyethyl methacrylate (HEMA) is a likely scenario of tobacco consuming dental patients. Possible modulating effects of nicotine in HEMA exposed cells are explored in this study.

Method: The human acute monocytic leukemia cell line, THP-1, was used as a model system. The cells were exposed to various combinations of HEMA and nicotine. Cell growth was monitored with flow cytometry. Cell death was measured with fluorescence microscopy. THP-1 monocytes were differentiated to THP-1 macrophages using 20 ng/ml phorbol myristate acetate (PMA), and during the differentiation cells attach to the cell culture dish. The MTT assay was used to measure cell attachment, thereby providing a coarse measure of cell differentiation. The differentiation was performed in the presence or absence of HEMA and nicotine.

Result: Exposure to HEMA resulted in altered THP-1 cell growth. This effect was not seen in samples exposed to HEMA in combination with nicotine and nicotine alone. Nicotine had no measurable effect on HEMA induced cell death. Cells incubated with PMA increased attachment of THP-1 cells. Co-incubation with HEMA increased the attachment. No effect was observed with HEMA and nicotine in combination.

Conclusion: Some HEMA induced effects on THP-1 cells is counteracted by nicotine. Further knowledge on the underlying mechanism is needed to understand the significance of the findings.

This abstract is based on research that was funded entirely or partially by an outside source: Norwegian Directorate of Health, Oslo, Norway.
Authors: JT Samuelsen1, V Ansteinsson2, KE Rakkestad3, R Becher4 and JE Dahl1.
Affiliation: 1NIOM – Nordic Institute of Dental Materials, Oslo, Norway. 2Department of Clinical Dentistry, University of Bergen, Faculty of Medicine and Dentistry, Bergen, Norway. 3Department of Pharmaceutical Biosciences, University of Oslo, Oslo, Norway. 4Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway.