The influence of glutathione on redox regulation by antioxidant proteins and apoptosis in macrophages exposed to 2-hydroxyethyl methacrylate (HEMA)

Krifka, Stephanie; Hiller, Karl‐Anton; Spagnuolo, Gianrico; Jewett, Anahid; Schmalz, Gottfried; Schweikl, Helmut

doi:10.1016/j.biomaterials.2012.04.013

Cited by 96 publications

(96 citation statements)

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“…The intracellular generation of ROS was determined using the oxidationsensitive fluorescent probe 2 0 7 0 -dichlorodihydrofluorescin diacetate (H 2 DCF-DA), while dihydroethidium (DHE) or dihydrorhodamine 123 (DHR123) were used for the detection of superoxide anions or hydrogen peroxide, respectively [17,24e27]. The cells were cultured in 6-well plates (5 Â 10 4 /well) for 48 h at 37 C. Then, the cells were exposed to HEMA (0-6-8 mM) or phorbol myristate acetate (0.0, 0.1 or 1.0 mM PMA) for 1 h or 24 h at 37 C as previously described [17]. PMA was used as a positive control substance to demonstrate induction of reactive oxygen species [28].…”

Section: Chemicals and Reagentsmentioning

confidence: 99%

“…We have recently shown that the expression of enzymatic antioxidants which directly metabolize ROS, like superoxide dismutase (SOD-1), glutathione peroxidase (GPx1/2) or catalase, was modified in HEMA-exposed cells depending on the availability of glutathione (GSH), a major non-enzymatic antioxidant [17]. These findings suggest that monomers may interfere and activate an even wider and more comprehensive system of antioxidative cell responses to completely control cellular redox balance.…”

Section: Introductionmentioning

confidence: 97%

“…To investigate these mechanisms, RAW264.7 mouse macrophages were established in recent projects as a suitable model cell line of the innate immune system [15,17]. Macrophages are in the first line of defense among those cells of the immune system infiltrating the dental pulp during progression of carious lesions.…”

Section: Introductionmentioning

confidence: 99%

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Activation of the Nrf2-regulated antioxidant cell response inhibits HEMA-induced oxidative stress and supports cell viability

et al. 2015

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Section: Chemicals and Reagentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Activation of the Nrf2-regulated antioxidant cell response inhibits HEMA-induced oxidative stress and supports cell viability

et al. 2015

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“…It has been largely reported that HEMA induces apoptosis in vitro after 24 h (Table 3) (Hanks et al 1991, Krifka et al 2012. Moreover, HEMA induces morphological changes in cultured cells, such as human pulp fibroblasts (HPFs) and human gingival epithelial cells.…”

Section: Hema-induced Apoptosis In Vitromentioning

confidence: 99%

“…Moreover, HEMA triggers the expression of stress-responsive genes at the transcriptional level through the accumulation of ROS. Krifka et al (2012) concluded that monomer-induced apoptosis is an active cell response to levels of ROS exceeding the cells' ability to maintain redox homeostasis. They hypothesized that cells differentially activate a balance network of enzymatic cellular antioxidants to control the intracellular oxidative state after exposure to HEMA monomer.…”

Section: Introductionmentioning

confidence: 99%

HEMA‐induced cytotoxicity: oxidative stress, genotoxicity and apoptosis

2014

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Gallorini M, Cataldi A, di Giacomo V. HEMA-induced cytotoxicity: oxidative stress, genotoxicity and apoptosis.International Endodontic Journal, 47, 813-818, 2014. Dental resin composites consist of organic polymers with inorganic fillers used as bonding resins and direct filling materials in dentine adhesives and as sealing agents for inlays, crowns and orthodontic brackets. Despite various modifications in the formulation, the chemical composition of composite resins includes inorganic filler particles and additives, which are incorporated into a mixture of an organic resin matrix. Among them, 2-hydroxyethylmethacrylate (HEMA) is one of the most frequently used. Several studies have attempted to clarify the mechanisms underlying HEMA cytotoxicity. Most of them support the hypothesis that this compound, once released in the oral environment, increases reactive oxygen species (ROS) production and oxidative DNA damage through double-strand breaks evidenced by in vitro presence of micronuclei. As a consequence, the glutathione detoxifying intracellular pool forms adducts with HEMA through its cysteine motif and inflammation begins to occur: transcription of early genes of inflammation such as tumour necrosis factor a or inducible cyclooxygenase up to the secretion of prostaglandins 2. These phenomena are counteracted by N-acetylcysteine (NAC), a nonenzymatic antioxidant, but not by vitamin E or other antioxidant. Consequently, NAC prevents HEMA-induced apoptosis acting as a direct ROS scavenger. This minireview collects the most significant papers on HEMA and tries to make an overview of its cytotoxicity on different cell types and experimental models.

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Effect of extremely low‐frequency electromagnetic fields on antioxidant activity in the human keratinocyte cell line NCTC 2544

Calcabrini

Mancini

Bellis

et al. 2016

Biotech and App Biochem

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Some epidemiological studies have suggested possible associations between exposure to extremely low-frequency electromagnetic fields (ELF-EMFs) and various diseases. Recently, ELF-EMF has been considered as a therapeutic agent. To support ELF-EMF use in regenerative medicine, in particular in the treatment of skin injuries, we investigated whether significant cell damage occurs after ELF-EMF exposure. Reactive oxygen species (ROS) production was evaluated in the human keratinocyte exposed for 1 H to 50 Hz ELF-EMF in a range of field strengths from 0.25 to 2 G. Significant ROS increases resulted at 0.5 and 1 G and under these flux densities ROS production, glutathione content, antioxidant defense activity, and lipid peroxidation markers were assessed for different lengths of time. Analyzed parameters of antioxidant defense and membrane integrity showed a different trend at two selected magnetic fluxes, with a greater sensitivity of the cells exposed to 0.5 G, especially after 1 H. All significant alterations observed in the first 4 H of exposure reverted to controls 24 H after suggesting that under these conditions, ELF-EMF induces a slight oxidative stress that does not overwhelm the metabolic capacity of the cells or have a cytotoxic effect.

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The influence of glutathione on redox regulation by antioxidant proteins and apoptosis in macrophages exposed to 2-hydroxyethyl methacrylate (HEMA)

Cited by 96 publications

References 50 publications

Activation of the Nrf2-regulated antioxidant cell response inhibits HEMA-induced oxidative stress and supports cell viability

Activation of the Nrf2-regulated antioxidant cell response inhibits HEMA-induced oxidative stress and supports cell viability

HEMA‐induced cytotoxicity: oxidative stress, genotoxicity and apoptosis

Effect of extremely low‐frequency electromagnetic fields on antioxidant activity in the human keratinocyte cell line NCTC 2544

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