Colloidal platinum nanoparticles increase mitochondrial stress induced by resin composite components.

Abstract

Components of dental composites have been implicated as metabolic and oxidative stressors in cells. Antioxidant colloidal platinum nanoparticles (CPtN) could be useful as nanofillers that reduce cellular stress caused during placement and exposure to unpolymerized composite components. Yet, CPtN may have pro- or anti-oxidative properties depending on the chemical environment in which they are used. This study investigated the ability of CPtN to mitigate mitochondrial or oxidative stress induced by camphorquinone (CQ) and dimethylaminoethyl methacrylate (DMAEM), two components of dental composites that initiate light-activated addition polymerization. THP-1 human monocytic cells were exposed to subtoxic concentrations of CQ and DMAEM, then blue light for 0-60 s. Mitochondrial and oxidative stress were estimated 0, 6, or 24 h after irradiation by measuring cellular ATP or GSH levels, respectively. CPtN (0-20 ppm) were added prior to blue light irradiation. Statistically significant effects were determined by ANOVA with Tukey post-hoc analysis (α = 0.05). Light alone did not alter THP-1 activity, but CQ and DMAEM induced 120% increases in cell ATP levels, which was increased further (50%) by CPtN. Blue light irradiation caused a 50% drop in ATP levels, which increased to 75% when CPtN were added. GSH levels were suppressed by CQ/DMAEM and blue light, and CPtN increased suppression by 20-30%. CPtN did not mitigate mitochondrial or oxidative stress in THP-1, but amplified these stresses under the conditions tested.