Effects of BisGMA on glutathione metabolism and apoptosis in human gingival fibroblasts in vitro

N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

“…Moreover, Eckhardt et al (2009) have found that 5 mM NAC was most protective against the cytotoxic effects of high concentrations of resin monomers, providing evidence for the use of 5 mM NAC in our study. In addition, we mainly concentrated on the cytotoxicity of Bis-GMA within the initial 24 h, which was in consistent with the time reported by Chang et al (2010b) and Engelmann et al (2004). No significant changes in cell viability were observed in cultures exposed to 0-0.1 mM Bis-GMA in the presence or absence of NAC after a 24 h exposure.…”

“…To investigate whether ROS generation is involved in Bis-GMA-induced cytotoxicity, HOKs were exposed to increasing concentrations of Bis-GMA and the ROS scavenger NAC. Considering the concentrations provided in previous study (Engelmann et al, 2004, Chang et al, 2010b and the concentrations patients might be exposed (Polydorou et al, 2007, Van Landuyt et al, 2011, 0.01-0.5 mM Bis-GMA concentrations were used. Moreover, Eckhardt et al (2009) have found that 5 mM NAC was most protective against the cytotoxic effects of high concentrations of resin monomers, providing evidence for the use of 5 mM NAC in our study.…”

Apototic and Necrotic Influence of Dental Resin Polymerization Initiators in Human Gingival Fibroblast Cultures

“…Recent reports have shown that resin-based dental materials caused cell death by apoptosis and necrosis in rat submandibular acinar cells and human endothelial cells 32,33) . The resin monomer Bis-GMA and comonomer TEGDMA augment apoptosis in dose-and time-dependent manners in HGF cells 34,35) . 4-N,N-dimethyl amino benzoic acid ethylester (DMABEE), which is a polymerization initiator, augments cell death via apoptosis and necrosis in human histiocytic lymphoma promonocytic cells in a concentration-dependent manner 36) .…”

Effects of HEMA on type I collagen protein in human gingival fibroblasts

“…A TC 50 concentration of HEMA ranging from 10 μmol/L to 10 mmol/L has been demonstrated, mainly by mitochondrial dehydrogenase activity (MTT assay) and lactate dehydrogenase activity (LDH assay). It has been demonstrated that HEMA can induce genotoxicity (Schweikl et al, 2005) and apoptosis (Janke et al, 2003;Mantellini et al, 2003;Engelmann et al, 2004;Spagnuolo et al, 2004;Paranjpe et al, 2005); it interferes with the cell cycle and DNA synthesis (Hanks et al, 1991;Chang et al, 2005), increases the production of reactive oxygen species (ROS) (Chang et al, 2005;Spagnuolo et al, 2006), and induces a strong depletion of intracellular glutathione level even after very short times of exposure (Volk et al, 2006). Many of these data have shown the cytotoxic effects of HEMA at concentrations near the TC 50 value while very few studies have demonstrated HEMA influence in cells exposed to minor toxic concentrations (Costa et al, 1999;Bouillaguet et al, 2000) and the effect of these monomers on the expression of specific proteins (About et al, 2002).…”