TEGDMA induces mitochondrial damage and oxidative stress in human gingival fibroblasts.

Free monomers including triethylene glycol dimethacrylate (TEGDMA) are released by resin composite. Recent studies in vitro have demonstrated that TEGDMA induced GSH depletion and production of radical oxygen species (ROS) in human gingival fibroblasts (HGF) but the exact mechanism of these events remains unclear. Our purpose is to investigate the origin of ROS production. TEGDMA induces a rapid (within 30 min) and drastic depletion of ATP concomitant with the GSH depletion. After 3h incubation, TEGDMA induced an increase of lipid peroxidation associated with LDH leakage. Our data also showed that TEGDMA produced damage at mitochondrial level. This is demonstrated by the collapse of mitochondrial membrane potential (MMP) in HGF treated with TEGDMA. The protective effect of carbonylcyanide m-chlorophenylhydrazone (CCCP), an uncoupler of oxidative phosphorylation on lipid peroxidation and LDH leakage suggests that mitochondria can be implicated in these events. Trolox, a soluble derivative of Tocopherol, weakly prevents ATP but not GSH depletion and totally protects the cells against lipid peroxidation, MMP collapse and cell death. Thus, the present results suggest that TEGDMA induces lipid peroxidation and mitochondrial damage, which contribute to cell death.