Blue light generates reactive oxygen species (ROS) differentially in tumor vs. normal epithelial cells.

ABSTRACT

OBJECTIVES: Blue light of high intensity is commonly used in dentistry to activate polymerization of resin restorative materials. Other than its effects on the retina, the biological effects of blue light (380-500nm wavelengths) are poorly studied. Limited evidence suggests that blue light acts by forming intracellular reactive oxygen species (ROS) that then affect critical cell functions. If the biological effects of blue light are redox-mediated, antioxidants might be used to mitigate unwanted side effects of blue light during clinical use, or blue light might be used therapeutically to modulate redox-sensitive cell signaling responses. METHODS: Intracellular ROS were estimated using HFLUOR-DA (dihydrofluorescein diacetate), a vital fluorescein-based, redox-sensitive dye. ROS were measured in normal (NHEK) and oral squamous carcinoma (OSC2) epithelial cells, shown previously to respond differentially to blue light irradiation. Two-hour cumulative levels of ROS and approximate ROS lifetimes were measured after irradiation doses of 5-30 J/cm(2). The blue light-induced generation of ROS was further tested by the ability of the antioxidants N-acetylcysteine (NAC) and vitamin E to mitigate intracellular ROS levels. RESULTS: Dose-dependent ROS levels were generated in both NHEK and OSC2 cells, but cumulative levels were higher and persisted longer in the OSC2 cells. Both vitamin E and NAC significantly reduced blue-light-induced levels of ROS, but were more effective in the OSC2 cells. SIGNIFICANCE: The induction of intracellular ROS by blue light implies that redox effects may mediate cellular responses to blue light. This result suggests the opportunity to mitigate any effects of direct or coincident exposure during dental treatment via antioxidants, and the opportunity to exploit differences in redox processing among cells for possible treatment of epithelial cancer or wound healing.