Mass spectrometry-based metabolomics study of nicotine exposure in THP-1 monocytes.

The tobacco alkaloid nicotine is known for its activation of neuronal nicotinic acetylcholine receptors. Nicotine is consumed in different ways such as through conventional smoking, e-cigarettes, snuff or nicotine pouches. The use of snuff has been associated with several adverse health effects, such as inflammatory reactions of the oral mucosa and oral cavity cancer.

Digital manufacturing techniques and the in vitro biocompatibility of acrylic-based occlusal device materials.

Objectives: Material chemistry and workflow variables associated with the fabrication of dental devices may affect the biocompatibility of the dental devices. The purpose of this study was to compare digital and conventional workflow procedures in the manufacturing of acrylic-based occlusal devices by assessing the cytotoxic potential of leakage products.

Methods: Specimens were manufactured by 3D printing (stereolithography and digital light processing), milling, and autopolymerization.

Investigation of biological effects of HEMA in 3D-organotypic co-culture models of normal and malignant oral keratinocytes.

Several studies utilizing 2-dimensional (2D) cell culture systems have linked 2-hydroxyethyl methacrylate (HEMA) with cytotoxic effects in oral mucosa and dental pulp cells. Although such studies are invaluable in dissecting the cellular and molecular effects of HEMA, there is a growing interest in the utilization of appropriate 3-dimensional (3D) models that mimic the structure of oral mucosa. Using a previously characterized 3D-organotypic co-culture model, this study aimed to investigate the cellular and molecular effects of HEMA on a 3D-co-culture model consisting of primary normal oral keratinocyte (NOK) grown directly on top of collagen I gel containing primary oral fibroblasts (NOF).

Biological aspects of modern dental composites.

Biological evaluation of resin-based dental composites has traditionally been based on in vitro endpoint tests with different methods to determine loss of cell viability and cell morphology changes after exposure to the material or monomer constituents. The data reveals a potential for biological effects, but clinical relevance of such data is limited. Positive allergy tests and allergic clinical reactions to dental monomers are observed in dental personnel and patients.

Ion release from three different dental alloys - effect of dynamic loading and toxicity of released elements.

The aims of this study were to assess if dynamic loading increases the metal ion release of selected dental alloys and to evaluate the cytotoxicity of the released metal ions. One Pd-Ag alloy (Aurolite 2B) and two Co-Cr alloys (Wirobond 280 and d.Sign 30) were investigated.

Establishing a macrophage model with relevance for oral methacrylate monomer exposures: Attenuated Staphylococcus aureus-induced cytokine release from human macrophages.

Background: Leakage of unpolymerized methacrylate monomers after placement of methacrylate-containing polymeric dental materials leads to human exposure. Based on studies using murine macrophages and LPS from Escherichia coli (E. coli), dental monomers like 2-hydroxyethyl methacrylate (HEMA) are known to inhibit lipopolysaccharide (LPS) induced cytokine release.

The dental monomer HEMA causes proteome changes in human THP-1 monocytes.

Resin-based biomaterials are widely used in medical and dental treatment, and both clinicians and patients are exposed to the materials. The knowledge of toxicity is mainly based on in vitro studies at exposure concentrations that induce cell death. However, severe cell damage and cell death signaling may overshadow essential cellular events caused by a possible toxicant.

The dental monomer 2-hydroxyethyl methacrylate (HEMA) causes transcriptionally regulated adaptation partially initiated by electrophilic stress.

Objectives: Cellular responses including cell death are induced by in vitro exposure to the un-polymerized dental monomer 2-hydroxyethyl methacrylate (HEMA). Activation of the Nrf2/ARE signaling pathway has been suggested to mediate the cellular responses. Activation of this pathway may occur either indirectly through generation of increased oxidative stress or through direct binding to cysteine thiols due to the electrophilic properties of HEMA.

Di-n-butyl phthalate modifies PMA-induced macrophage differentiation of THP-1 monocytes via PPARγ.

The present study examined the effects of di-n-butyl phthalate (DBP) on phorbol myristate acetate (PMA)-induced macrophage differentiation of THP-1 monocytes, determined by morphological classification and flow cytometry. Focusing on the expression of the surface marker CD36, the potential role of peroxisome proliferator-activated receptor gamma (PPARγ) was examined using various PPARγ agonists and antagonists. As the PPARγ ligand-binding domain contains multiple ligand-binding sites (LBS), agonist and antagonists targeting the different sites were used.

The dental monomer hydroxyethyl methacrylate (HEMA) counteracts lipopolysaccharide-induced IL-1β release-Possible role of glutathione.

Methacrylate monomers, like 2-hydroxyethyl methacrylate (HEMA), are common components of resin based dental materials. Leakage of unpolymerized monomers after placement and curing leads to human exposure. HEMA is known to inhibit lipopolysaccharide (LPS) induced cytokine release.

Automatic Quiz Generation for the Elderly.

According to the literature, ageing causes declines in sensory, perceptual, motor and cognitive abilities. The combination of reduced vision, hearing, memory and mobility contributes to isolation and depression. We argue that memory games have potential for enhancing the cognitive ability of the elderly and improving their life quality.

Cell toxicity of 2-hydroxyethyl methacrylate (HEMA): the role of oxidative stress.

2-Hydroxyethyl methacrylate (HEMA) is a methacrylate monomer used in polymer-based dental-restorative materials. In this study, the viability of human lung epithelial cells, BEAS-2B, was investigated after exposure to this monomer. Exposure to HEMA reduced the viability of the BEAS-2B cells as a result of increased apoptosis, interruption of the cell cycle, and decreased cell proliferation.

TEGDMA and filler particles from dental composites additively attenuate LPS-induced cytokine release from the macrophage cell line RAW 264.7.

Objectives: Due to incomplete curing and material degradation, cells in the oral cavity may be exposed to monomers and filler particles from dental composite fillings. The objective of the present study was to investigate if combined exposures to particles and a methacrylate monomer from composite fillings resulted in additive effects on the macrophage immune response.

Material And Methods: Two filler particles, Nanosilica (12 nm) and Quartz (1 μm), were studied at concentrations 0.

Cell toxicity of methacrylate monomers-the role of glutathione adduct formation.

Polymer-based dental restorative materials are designed to polymerize in situ. However, the conversion of methacrylate monomer to polymer is never complete, and leakage of the monomer occurs. It has been shown that these monomers are toxic in vitro; hence concerns regarding exposure of patients and dental personnel have been raised.

Dental monomers inhibit LPS-induced cytokine release from the macrophage cell line RAW264.7.

Methacrylate monomers have been identified in aqueous extracts of freshly cured dental fillings. The hypothesis tested presently was that low concentrations of triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) alone or in combination interfere with the LPS-induced release of cytokines from the macrophage cell line RAW264.7.

Mono-2-ethylhexylphthalate (MEHP) induces TNF-α release and macrophage differentiation through different signalling pathways in RAW264.7 cells.

Epidemiological studies have associated indoor phthalate exposure with increased incidences and severity of asthma in children and adults, and inflammatory effects have been suggested as a possible mechanism. Recent studies report that phthalates may activate mitogen-activated protein (MAP) kinase p38 and various peroxisome proliferator-activated receptor (PPAR) isoforms. Here we confirm and extend these findings by investigating possible signalling pathways activated in the murine monocyte-macrophage cell line RAW264.

Biotransformation enzymes and lung cell response to 2-hydroxyethyl-methacrylate.

The aim of this in vitro study was to investigate possible involvement of cytochrome P450 (CYP) enzymes in modifying the toxic potential of 2-hydroxyethyl-methacrylate (HEMA). Primary cultures of CYP expressing rat alveolar type 2 cells were exposed to varying concentrations of HEMA. Nuclear translocation of aryl hydrocarbon receptor (AhR) after HEMA exposure (100 μM) was demonstrated by immunocytochemical staining.

DNA-damage, cell-cycle arrest and apoptosis induced in BEAS-2B cells by 2-hydroxyethyl methacrylate (HEMA).

The methacrylate monomer 2-hydroxyethyl methacrylate (HEMA) is commonly used in resin-based dental restorative materials. These materials are cured in situ and HEMA and other monomers have been identified in ambient air during dental surgery. In vitro studies have demonstrated a toxic potential of methacrylates, and concerns have been raised regarding possible health effects due to inhalation.

Role of thiol-complex formation in 2-hydroxyethyl- methacrylate-induced toxicity in vitro.

Methacrylate monomers that are found to leach from cured resin-based dental materials induce biological effects in vitro. The underlying mechanisms have not been fully elucidated although involvement of increased cellular reactive oxygen species (ROS) and DNA-damage has been suggested. In this in vitro study we have elucidated the impact of a commonly used methacrylate monomer, HEMA, on the level and oxidation state of cellular glutathione, intracellular ROS level, as well as the formation of complex between HEMA and glutathione.

DNA damage and DNA damage responses in THP-1 monocytes after exposure to spores of either Stachybotrys chartarum or Aspergillus versicolor or to T-2 toxin.

We have characterized cell death in THP-1 cells after exposure to heat-treated spores from satratoxin G-producing Stachybotrys chartarum isolate IBT 9631, atranone-producing S. chartarum isolate IBT 9634, and sterigmatocystin-producing Aspergillus versicolor isolate IBT 3781, as well as the trichothecenes T-2 and satratoxin G. Spores induced cell death within 3-6 h, with Stachybotrys appearing most potent.

Filler particles used in dental biomaterials induce production and release of inflammatory mediators in vitro.

Although dental composites are in extensive use today, little is known about the biological effects of the filler particles. As composite materials are gradually broken down in the aggressive environment of the oral cavity, the filler particles may leak and induce toxic effects on the surrounding tissue and cells. The aim of this study was to elucidate possible adverse biological effects of commonly used dental filler particles; bariumaluminiumsilica (BaAlSi) and bariumaluminiumfluorosilica (BaAlFSi) with mean size of 1 microm.

HEMA reduces cell proliferation and induces apoptosis in vitro.

Objectives: Methacrylate monomers have been identified in aqueous extracts of freshly cured compomers. Both cells in the pulpal cavity and various cells of the oral mucosa can potentially be exposed to these leachables. Short-term exposure to dental monomers at relatively high concentrations induces adverse biological effects in vitro.