IADR Abstract Archives
Ascorbic acid modulates the expression of antioxidant enzymes induced by HEMA and TEGDMA
Objectives: To evaluate the effect of ascorbic acid (AA) on the expression of the enzymes catalase (CAT) and hemo-oxygenase-1 (HO-1) in response to the increase of Reactive Oxygen Species (ROS) by exposure to 2-Hydroxyethyl methacrylate (HEMA) and Triethylene glycol dimethacrylate (TEGDMA) in odontoblast-like cells.
Methods: The expression of CAT and HO-1 transcripts was evaluated by qPCR after exposing the cells to 3, 6 and 12 mM HEMA and to 1.5, 3 and 6 mM TEGDMA for 3, 9 and 18 h. The expression values were compared with the negative control (unexposed cells) and with the expression induced by the positive control (hydrogen peroxide). The role of the AA on the expression of antioxidant enzymes was corroborated incubating AA simultaneously with HEMA or TEGDMA.
Results: HEMA and TEGDMA are ROS generating monomers, which induce a transient increase of intracellular oxygen intermediates, which leads to cells to overexpress CAT and HO-1 as a redox-regulated response. In the first 3 hours of contact with HEMA and TEGDMA, CAT expression was upregulated as early defense line against oxidative stress in cells exposed. Overexpression of the stress-inducible HO-1 enzyme caused by HEMA and TEGDMA may indicate the need for additional antioxidants. AA stimulated CAT and HO-1 expression, since it induced overexpression from 3 h exposure regarding to the expression induced by hydrogen peroxide.
Conclusions: AA, like an antioxidant molecule, plays a cytoprotective role against the oxidative stress induced by the monomers, regulating the expression of CAT and HO-1. AA has been recognized as an active modulator of cell signaling through the activation of transcription factors sensitive to oxidative stress. This process could function as a mechanism for the preservation of cell viability by controlling several of the oxidative factors that induce cellular injury related to monomers exposure.
Methods: The expression of CAT and HO-1 transcripts was evaluated by qPCR after exposing the cells to 3, 6 and 12 mM HEMA and to 1.5, 3 and 6 mM TEGDMA for 3, 9 and 18 h. The expression values were compared with the negative control (unexposed cells) and with the expression induced by the positive control (hydrogen peroxide). The role of the AA on the expression of antioxidant enzymes was corroborated incubating AA simultaneously with HEMA or TEGDMA.
Results: HEMA and TEGDMA are ROS generating monomers, which induce a transient increase of intracellular oxygen intermediates, which leads to cells to overexpress CAT and HO-1 as a redox-regulated response. In the first 3 hours of contact with HEMA and TEGDMA, CAT expression was upregulated as early defense line against oxidative stress in cells exposed. Overexpression of the stress-inducible HO-1 enzyme caused by HEMA and TEGDMA may indicate the need for additional antioxidants. AA stimulated CAT and HO-1 expression, since it induced overexpression from 3 h exposure regarding to the expression induced by hydrogen peroxide.
Conclusions: AA, like an antioxidant molecule, plays a cytoprotective role against the oxidative stress induced by the monomers, regulating the expression of CAT and HO-1. AA has been recognized as an active modulator of cell signaling through the activation of transcription factors sensitive to oxidative stress. This process could function as a mechanism for the preservation of cell viability by controlling several of the oxidative factors that induce cellular injury related to monomers exposure.