Retinal damage induced by commercial light emitting diodes (LEDs)

Spectra of “white LEDs” are characterized by an intense emission in the blue region of the visible spectrum, absent in daylight spectra. This blue component and the high intensity of emission are the main sources of concern about the health risks of LEDs with respect to their toxicity to the eye and...

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Veröffentlicht in:Free radical biology & medicine 2015-07, Vol.84, p.373-384
Hauptverfasser: Jaadane, Imene, Boulenguez, Pierre, Chahory, Sabine, Carré, Samuel, Savoldelli, Michèle, Jonet, Laurent, Behar-Cohen, Francine, Martinsons, Christophe, Torriglia, Alicia
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Sprache:eng
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Zusammenfassung:Spectra of “white LEDs” are characterized by an intense emission in the blue region of the visible spectrum, absent in daylight spectra. This blue component and the high intensity of emission are the main sources of concern about the health risks of LEDs with respect to their toxicity to the eye and the retina. The aim of our study was to elucidate the role of blue light from LEDs in retinal damage. Commercially available white LEDs and four different blue LEDs (507, 473, 467, and 449nm) were used for exposure experiments on Wistar rats. Immunohistochemical stain, transmission electron microscopy, and Western blot were used to exam the retinas. We evaluated LED-induced retinal cell damage by studying oxidative stress, stress response pathways, and the identification of cell death pathways. LED light caused a state of suffering of the retina with oxidative damage and retinal injury. We observed a loss of photoreceptors and the activation of caspase-independent apoptosis, necroptosis, and necrosis. A wavelength dependence of the effects was observed. Phototoxicity of LEDs on the retina is characterized by a strong damage of photoreceptors and by the induction of necrosis. [Display omitted] •LED light induces oxidative stress and retinal injury.•LED light induces photoreceptor death by necrosis and apoptosis.•The blue component of LED is the major cause of retinal damage.
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2015.03.034