title: 670 nm light mitigates oxygen-induced degeneration in C57BL/6J mouse retina.
abstract: BACKGROUND
  Irradiation with light wavelengths from the far red (FR) to the near infrared (NIR) spectrum (600 nm -1000 nm) has been shown to have beneficial effects in several disease models. In this study, we aim to examine whether 670 nm red light pretreatment can provide protection against hyperoxia-induced damage in the C57BL/6J mouse retina. Adult mice (90-110 days) were pretreated with 9 J/cm2 of 670 nm light once daily for 5 consecutive days prior to being placed in hyperoxic environment (75% oxygen). Control groups were exposed to hyperoxia, but received no 670 nm light pretreatment. Retinas were collected after 0, 3, 7, 10 or 14 days of hyperoxia exposure (n = 12/group) and prepared either for histological analysis, or RNA extraction and quantitative polymerase chain reaction (qPCR). Photoreceptor damage and loss were quantified by counting photoreceptors undergoing cell death and measuring photoreceptor layer thickness. Localization of acrolein, and cytochrome c oxidase subunit Va (Cox Va) were identified through immunohistochemistry. Expression of heme oxygenase-1 (Hmox-1), complement component 3 (C3) and fibroblast growth factor 2 (Fgf-2) genes were quantified using qPCR.
  
  
  RESULTS
  The hyperoxia-induced photoreceptor loss was accompanied by reduction of metabolic marker, Cox Va, and increased expression of oxidative stress indicator, acrolein and Hmox-1. Pretreatment with 670 nm red light reduced expression of markers of oxidative stress and C3, and slowed, but did not prevent, photoreceptor loss over the time course of hyperoxia exposure.
  
  
  CONCLUSIONS
  The damaging effects of hyperoxia on photoreceptors were ameliorated following pretreatment with 670 nm light in hyperoxic mouse retinas. These results suggest that pretreatment with 670 nm light may provide stability to photoreceptors in conditions of oxidative stress.
authors.affiliation: ARC Centre of Excellence in Vision Science and John Curtin School of Medical Research, 131 Garran Road, Canberra, ACT 0200, Australia. rizalyn.albarracin@anu.edu.au.
authors.forename: Rizalyn
authors.initials: R
authors.lastname: Albarracin
authors.forename: Riccardo
authors.initials: R
authors.lastname: Natoli
authors.forename: Matthew
authors.initials: M
authors.lastname: Rutar
authors.forename: Krisztina
authors.initials: K
authors.lastname: Valter
authors.forename: Jan
authors.initials: J
authors.lastname: Provis
mesh_terms: D000818:Animals; D002470:Cell Survival / Q000528:radiation effects; D005260:Female; D018496:Hyperoxia / Q000150:complications* / Q000378:metabolism; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007259:Infrared Rays; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018613:Microscopy, Confocal; D018384:Oxidative Stress / Q000528:radiation effects*; D020419:Photoreceptor Cells, Vertebrate / Q000473:pathology / Q000528:radiation effects*; D060888:Real-Time Polymerase Chain Reaction; D012160:Retina / Q000473:pathology / Q000528:radiation effects; D012162:Retinal Degeneration / Q000209:etiology / Q000378:metabolism / Q000473:pathology*