Blue light differentially alters cellular redox properties

• Published in: Journal of biomedical materials research 2005-02, Vol.72B (2), p.223-229
• Main Authors: Lewis, Jill B., Wataha, John C., Messer, Regina L. W., Caughman, Gretchen B., Yamamoto, Tetsuya, Hsu, Stephen D.
• Format: Article
• Language: English
• Subjects: apoptosis; Apoptosis - radiation effects; Cell Survival - radiation effects; Cells, Cultured; Dose-Response Relationship, Radiation; Humans; Keratinocytes - metabolism; Keratinocytes - radiation effects; Light; Mitochondrial Proteins - analysis; Mitochondrial Proteins - radiation effects; oral tumor cells; Oxidation-Reduction - radiation effects; Oxidative Stress; Proteins - analysis; Proteins - radiation effects; proteomics; Reactive Oxygen Species - metabolism; Reactive Oxygen Species - radiation effects; Succinate Dehydrogenase - metabolism; Succinate Dehydrogenase - radiation effects; visible light
• ISSN: 1552-4973; 0021-9304; 1552-4981
• DOI: 10.1002/jbm.b.30126

Blue light (λ = 380–500 nm) historically has been used to initiate polymerization of biomaterials and recently has been proposed as a therapeutic agent. New evidence suggests that cell‐type–specific responses result from redox changes induced by exposure to blue light. Cultured cells were exposed to defined doses of blue light, equivalent to exposure times of 10 s and 2 min, to achieve energies of 5 J/cm2 and 60 J/cm2, respectively, after which (a) viable cell number, (b) cellular protein profiles, (c) mitochondrial succinate dehydrogenase (SDH) activity, (d) total reactive oxygen species (ROS), and (e) induction of apoptosis were compared to that of nonexposed control cultures. Results showed that blue‐light exposure arrested monocyte cell growth and increased levels of peroxiredoxins. SDH activity of normal epidermal keratinocytes (NHEK) was slightly enhanced by blue light, whereas identical treatment of OSC2 oral tumor cells resulted in significant suppression of SDH activity. Blue‐light exposure generally induced higher levels of total ROS in OSC2 cells than in NHEK. Finally, only OSC2 cells exhibited signs of apoptosis via Annexin V staining following exposure to blue light. These data support the central hypothesis that blue light induces an oxidative stress response in cultured cells resulting in cell‐type–specific survival outcomes. The identification of oxidative stress as a mediator of the effects of blue light is a critical first step in defining its biological risks and therapeutic opportunities. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 72B: 223–229, 2005