Composite resins were introduced in the 1960s for the restoring of anterior teeth in substitution of the amalgam that presented both aesthetical and biocompatibility problems. However, since the polymerization of methacrylates is never complete, it became evident the necessity to appraise the biocompatibility of composite resins. The incomplete conversion causes in fact the release of monomers that may implement adverse effects in the organism, i.e. allergic reactions, systemic toxicity, cytotoxicity, estrogenicity and mutagenicity. Because very little information has been so far delivered on the consequences of methacrylic monomers on cell metabolism, we were driven to investigate the biochemical interactions between methacrylates and human cells. The present work summarizes the effects of TEGDMA, UDMA, BDDMA, HEMA and Bis-GMA on 1) cellular energetic metabolism (oxygen consumption rate, glucose consumption, G6PDH, lactate production) and 2) cellular redox status (GSH concentration, and the activity of the enzymes regulating glutathione metabolism). The results obtained showed that all monomers induced both cellular differentiation and a decrease of oxygen consumption. Moreover, cells treated with TEGDMA and HEMA showed a significant enhancement of glucose consumption and lactate production, induced GSH depletion and stimulated G6PDH and GR activity. BDDMA also induced GSH depletion but without any effect on the activity of the enzymes involved in glutathione metabolism, while UDMA did not change GSH content and redox metabolism at all. The mechanism of the differentiating action can be basically reconducted to an impairment of the mitochondrial respiration which starts 2 hours after incubation of the cells with each monomer and determines in the following hours an increase of anaerobic glycolysis. Thus the changes in energy metabolism and glutathione redox balance could be considered a potential mechanism for inducing clinical and sub-clinical adverse effects and thus providing a wider look for testing biocompatibility of dental materials.
Nocca, G., Martorana, G. E., De Sole, P., Gambarini, G., Giardina, B., Calla', C. A. M., Lupi, A., effects of methacrylates present in dental composite resins on HL-60 cells metabolism, in Kaminsk, K., Dupoi, D. (ed.), dental material research, HD Kaminski and Easton A. DuPois, New York 2009: 101- 114 [http://hdl.handle.net/10807/4736]
effects of methacrylates present in dental composite resins on HL-60 cells metabolism
Nocca, Giuseppina;Martorana, Giuseppe Ettore;De Sole, Pasquale;Giardina, Bruno;Calla', Cinzia Anna Maria;Lupi, Alessandro
2009
Abstract
Composite resins were introduced in the 1960s for the restoring of anterior teeth in substitution of the amalgam that presented both aesthetical and biocompatibility problems. However, since the polymerization of methacrylates is never complete, it became evident the necessity to appraise the biocompatibility of composite resins. The incomplete conversion causes in fact the release of monomers that may implement adverse effects in the organism, i.e. allergic reactions, systemic toxicity, cytotoxicity, estrogenicity and mutagenicity. Because very little information has been so far delivered on the consequences of methacrylic monomers on cell metabolism, we were driven to investigate the biochemical interactions between methacrylates and human cells. The present work summarizes the effects of TEGDMA, UDMA, BDDMA, HEMA and Bis-GMA on 1) cellular energetic metabolism (oxygen consumption rate, glucose consumption, G6PDH, lactate production) and 2) cellular redox status (GSH concentration, and the activity of the enzymes regulating glutathione metabolism). The results obtained showed that all monomers induced both cellular differentiation and a decrease of oxygen consumption. Moreover, cells treated with TEGDMA and HEMA showed a significant enhancement of glucose consumption and lactate production, induced GSH depletion and stimulated G6PDH and GR activity. BDDMA also induced GSH depletion but without any effect on the activity of the enzymes involved in glutathione metabolism, while UDMA did not change GSH content and redox metabolism at all. The mechanism of the differentiating action can be basically reconducted to an impairment of the mitochondrial respiration which starts 2 hours after incubation of the cells with each monomer and determines in the following hours an increase of anaerobic glycolysis. Thus the changes in energy metabolism and glutathione redox balance could be considered a potential mechanism for inducing clinical and sub-clinical adverse effects and thus providing a wider look for testing biocompatibility of dental materials.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.