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. Author manuscript; available in PMC: 2015 May 28.
Published in final edited form as: Sci Transl Med. 2014 May 28;6(238):238ra69. doi: 10.1126/scitranslmed.3008234

Fig. 2. LPL treatment generates ROS in mammalian cells in vitro.

Fig. 2

(A) Mv1Lu cells were treated with LPL at various fluences and assessed for superoxide generation with MitoSOX Red. Mitochondria were counterstained with MitoTracker Green. Red and green overlays are shown representative of three independent experiments. Some cells were preincubated with NAC (1 mM) before LPL (3 J/cm2) treatment or antimycin A treatment as a positive control. Scale bars, 20 μm. (B) Superoxide generation after LPL (3 J/cm2) treatment of Mv1Lu cells. Data are means ± SD (n = 3). P value determined by two-tailed t test. (C) H2O2 generation in Mv1Lu cells (revealed by CM-H2DCFDA) in response to LPL irradiation, with or without NAC (1 mM). Mitochondria were counterstained with MitoTracker Red. Red and green overlays are shown. Scale bar, 100 μm. (D) Griess assay for NO generation after LPL (3 J/cm2) treatment of Mv1Lu cells and mouse dental papilla cells (MDPC-23). (E) H2O2 generation assessed with Amplex UltraRed after LPL treatment of FBS at various fluences. Some samples were preincubated with NAC (1 mM) before LPL treatment. (F) LPL (3 J/cm2)–induced generation of hydroxyl radicals in cell-free serum, as assessed with proxylhydroxylamine. In (D) to (F), data are means ± SD (n = 3). P values determined by two-tailed t test. These findings indicate that LPL treatment induces tertiary dentin formation within the rat tooth pulp.