Objectives: Blue light (380-500 nm) has been proposed as an oral cancer therapy based on the apoptotic responses of epithelial tumor cells to doses that have little effect on normal keratinocytes. Recent reports have suggested that the cellular response to blue light is mediated by reactive oxygen species (ROS) that are formed when blue light interacts with flavins in the extracellular matrix. These reports suggest that normal and tumor cells respond differently to ROS because these cells process ROS differently. Our previously published work supports the hypothesis that there also is an important role for intracellular changes induced by blue light and that these changes affect how cells respond to ROS generated extracellularly. Methods: We exposed human oral squamous cell carcinoma cells (OSC2, n=3 per condition) to blue light (0, 5, 30, 60 J/cm2) in a low-flavin medium that minimized extracellularly generated ROS. Hydrogen peroxide was then added (or not) immediately after light exposure at a sublethal dose (200 µM, pilot study), and succinate dehydrogenase activity of the cells was assessed 72 h post-light exposure as a measure of cell response. Results: We found that either blue light or 200µM hydrogen peroxide alone had minimal effects on OSC2 in low-flavin medium (<10% suppression), but the combination of the two nearly completely (>90%) suppressed succinate dehydrogenase activity at 30, 60 J/cm2. Conclusion: Because ROS generated in the medium were minimized and peroxide doses were sublethal by design, we conclude that for OSC2 cells, intracellular changes induced by blue light play a role in the management of oxidative stress produced by extracellularly generated ROS. Our future studies will focus on how cell cycle and survival pathways in normal and tumor cells are differentially affected by blue light and how these differences can be exploited therapeutically for oral cancer treatment.

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