Objective: Various protective effects of N-acetylcysteine (NAC) against triethylene glycol dimethacrylate (TEGDMA)-induced cell damage have been demonstrated, but so far there is no evidence on NAC direct monomer detoxification mechanism. Here, we hypothesized that NAC might reduce TEGDMA cytotoxicity due to direct NAC adduct formation. Method: we measured the cytotoxic effects of TEGDMA in presence and in absence of NAC by MTT test. Then we analyzed the presence of TEGDMA-NAC adduct formation in extracellular and intracellular compartments by capillary electrophoresis-UV detection (CE-UV) and capillary electrophoresis–mass spectrometry (CE-MS) analytical techniques. Moreover, we quantified the effective intracellular and extracellular TEGDMA concentrations through HPLC in the presence and absence of 10 mmol/L NAC. Data from all experiments were summarized as means ± standard deviation (SD) and differences between means were analyzed by one-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons. The level of significance was set at p<0.05. Result: TEGDMA reduced 3T3 cell vitality in a dose- and time-dependent manner, while NAC significantly decreased monomer cytotoxicity and extracellular monomer concentrations by a direct reaction with TEGDMA. The adducts between the two molecules were detected both in the presence and absence of cell. Conclusion: Our results suggest that in vitro detoxification capability of NAC against TEGDMA-induced cell damage might occur also through the formation of NAC-TEGDMA adduct.
TEGDMA Cytotoxicity and Direct Detoxification by NAC / Spagnuolo, G; Desiderio, C; Schweikl, H; Riccitiello, Francesco; Lupi, A; Rengo, S; Nocca, G.. - (2013). (Intervento presentato al convegno Annual Meeting of the IADR Continental European Division 2013 nel September 4-7, 2013).
TEGDMA Cytotoxicity and Direct Detoxification by NAC
RICCITIELLO, FRANCESCO;RENGO S;
2013
Abstract
Objective: Various protective effects of N-acetylcysteine (NAC) against triethylene glycol dimethacrylate (TEGDMA)-induced cell damage have been demonstrated, but so far there is no evidence on NAC direct monomer detoxification mechanism. Here, we hypothesized that NAC might reduce TEGDMA cytotoxicity due to direct NAC adduct formation. Method: we measured the cytotoxic effects of TEGDMA in presence and in absence of NAC by MTT test. Then we analyzed the presence of TEGDMA-NAC adduct formation in extracellular and intracellular compartments by capillary electrophoresis-UV detection (CE-UV) and capillary electrophoresis–mass spectrometry (CE-MS) analytical techniques. Moreover, we quantified the effective intracellular and extracellular TEGDMA concentrations through HPLC in the presence and absence of 10 mmol/L NAC. Data from all experiments were summarized as means ± standard deviation (SD) and differences between means were analyzed by one-way analysis of variance (ANOVA) followed by Tukey’s test for multiple comparisons. The level of significance was set at p<0.05. Result: TEGDMA reduced 3T3 cell vitality in a dose- and time-dependent manner, while NAC significantly decreased monomer cytotoxicity and extracellular monomer concentrations by a direct reaction with TEGDMA. The adducts between the two molecules were detected both in the presence and absence of cell. Conclusion: Our results suggest that in vitro detoxification capability of NAC against TEGDMA-induced cell damage might occur also through the formation of NAC-TEGDMA adduct.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.