title: Extracellular environment as one mediator of blue light-induced mitochondrial suppression.
abstract: OBJECTIVE
  The current study tested the hypothesis that the extracellular environment mediates mitochondrial suppression of oral epithelial cells and fibroblasts by blue light.
  
  
  METHODS
  We exposed Balb fibroblasts (Balb), normal human epidermal keratinocytes (NHEK), and oral squamous carcinoma cells (OSC2) to blue light (30-120J/cm2) in different cell-culture media and in phosphate buffered saline (PBS). Mitochondrial activity (MTT method) was used to assess cellular response 72 h post-light exposure. Cell-culture media were replaced or supplemented before or after light exposure to assess the variables of exposure time and medium degradation as mediators of blue light-induced effects.
  
  
  RESULTS
  Mitochondrial activity of NHEK was not suppressed by exposure to blue light regardless of extracellular conditions. The mitochondrial activity of OSC2 and Balb cells was suppressed most when cells were exposed to light in cell-culture medium (versus PBS). Blue light suppressed mitochondrial activity more when irradiated medium remained in contact with the cells at least 1h, indicating a time-dependence of the medium effects. Neither a replacement nor a supplementation of medium components reduced blue light-induced mitochondrial suppression.
  
  
  CONCLUSIONS
  Our results suggest that tissue environments influence cellular responses to blue light and that these environments should be considered when assessing any biological effects of blue light during the photopolymerization of restorative resins.
authors.affiliation: Department of Oral Biology and Maxillofacial Biology, Medical College of Georgia, Augusta, GA 30912-1100, USA.
authors.forename: Shaun
authors.initials: S
authors.lastname: Rotenberg
authors.forename: Jill B
authors.initials: JB
authors.lastname: Lewis
authors.forename: Petra E
authors.initials: PE
authors.lastname: Lockwood
authors.forename: Wan Y
authors.initials: WY
authors.lastname: Tseng
authors.forename: Regina L W
authors.initials: RL
authors.lastname: Messer
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Hsu
authors.forename: Yo
authors.initials: Y
authors.lastname: Omata
authors.forename: John C
authors.initials: JC
authors.lastname: Wataha
mesh_terms: D000818:Animals; D002021:Buffers; D002294:Carcinoma, Squamous Cell / Q000648:ultrastructure; D002460:Cell Line; D045744:Cell Line, Tumor; D004396:Coloring Agents / Q000494:pharmacology; D003470:Culture Media / Q000528:radiation effects; D004307:Dose-Response Relationship, Radiation; D004847:Epithelial Cells / Q000528:radiation effects; D005347:Fibroblasts / Q000528:radiation effects; D006801:Humans; D015603:Keratinocytes / Q000528:radiation effects; D008027:Light; D051379:Mice; D008807:Mice, Inbred BALB C; D008928:Mitochondria / Q000528:radiation effects*; D009062:Mouth Neoplasms / Q000648:ultrastructure; D010637:Phenolsulfonphthalein / Q000494:pharmacology; D010710:Phosphates; D017319:Photosensitizing Agents / Q000494:pharmacology; D012256:Riboflavin / Q000494:pharmacology; D012965:Sodium Chloride; D013385:Succinate Dehydrogenase / Q000528:radiation effects; D013997:Time Factors
chemical_list: D002021:Buffers; D004396:Coloring Agents; D003470:Culture Media; D010710:Phosphates; D017319:Photosensitizing Agents; D012965:Sodium Chloride; D013385:Succinate Dehydrogenase; D010637:Phenolsulfonphthalein; D012256:Riboflavin