Open AccessEffects of white light‐emitting diode ( LED ) exposure on retinal pigment epithelium in vivo
Author(s) -
Jaadane Imene,
Villalpando Rodriguez Gloria Elisa,
Boulenguez Pierre,
Chahory Sabine,
Carré Samuel,
Savoldelli Michèle,
Jonet Laurent,
BeharCohen Francine,
Martinsons Christophe,
Torriglia Alicia
Publication year - 2017
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13255
Subject(s) - retinal pigment epithelium , in vivo , white light , retinal , pigment , epithelium , white (mutation) , microbiology and biotechnology , optics , chemistry , biology , ophthalmology , materials science , optoelectronics , medicine , pathology , physics , biochemistry , genetics , organic chemistry , gene
Ageing and alteration of the functions of the retinal pigment epithelium ( RPE ) are at the origin of lost of vision seen in age‐related macular degeneration ( AMD ). The RPE is known to be vulnerable to high‐energy blue light. The white light‐emitting diodes ( LED ) commercially available have relatively high content of blue light, a feature that suggest that they could be deleterious for this retinal cell layer. The aim of our study was to investigate the effects of “white LED ” exposure on RPE . For this, commercially available white LED s were used for exposure experiments on Wistar rats. Immunohistochemical stain on RPE flat mount, transmission electron microscopy and Western blot were used to exam the RPE . LED ‐induced RPE damage was evaluated by studying oxidative stress, stress response pathways and cell death pathways as well as the integrity of the outer blood–retinal barrier ( BRB ). We show that white LED light caused structural alterations leading to the disruption of the outer blood–retinal barrier. We observed an increase in oxidized molecules, disturbance of basal autophagy and cell death by necrosis. We conclude that white LED s induced strong damages in rat RPE characterized by the breakdown of the BRB and the induction of necrotic cell death.