Exposure Limit Values (ELV) for artificial lighting were defined in order to prevent light-induced damage to the retina. the evaluation of the lighting devices include the correction of their spectra by the B(λ) function or blue light hazard function, representing the relative spectral sensitivity of the human eye to the blue light. This weighting function peaks between 435 and 440 nm. In this study we evaluate a new generation of light emitting diode (LED), the GaN-on-GaN (gallium nitride on gallium nitride) LED, that present an emission peak in the purple part of the spectrum. Wistar rats were exposed to GaN-on-GaN and conventional diodes at different retinal doses (from 2.2 to 0.5 J/cm 2). We show that GaN-on-GaN diodes are more toxic than conventional LED for the rat neural retina and the rat retinal pigment epithelium, indicating that the BLH (blue light hazard) weighting is not adapted to this type of diodes. One of the reasons of this increased toxicity is the effects of shorter wavelengths on mitochondria polarization. We also show that the threshold of phototoxic retinal dose in the rat (fixed at 11 J/cm 2 , BLH weighted) is overestimated, suggesting that the values used for regulations, calculated in primates using the same methods than in rats, should be revised. Exposure Limit Values (ELV), proposed by the ICNIRP (International Commission for Non-Ionizing Radiation Protection) were defined in order to prevent light-induced photochemical damage to the retina (blue light hazard). These limits were used in the EN NF 62471 standard that define four groups of photobiological risk for incoherent (non laser) light sources ranging from risk group 0, concerning light sources delivering a retinal dose up to 2.2 J/cm 2 in 10 000 s, that are thought to be no risk, to risk group 3 for which an exposure of 0.25 s or less might be harmful for the retina. It is worth noticing that the retinal dose corresponds to the amount of blue light reaching the retina. Actually, the spectra of the measured lighting devices is corrected using the B(λ) function. The B(λ) function, also called the blue light hazard function represents the relative spectral sensitivity of the human eye to the blue light hazard. It is based upon the relative spectral effectiveness of optical radiation to induce retinal photochemical injury (photic maculopathy) 1,2. This weighting function peaks near 445 nm and has a profile close to the sensitivity of shortwave cones. The attenuation of sensitivity for shorter wavelength visible light (<440 nm) is caused by the absorption of the lens of the eye and the cornea 3. Most of currently used LED are Gallium Nitride-based (GaN) grown on top of sapphire or silicon substrate. In the last few years a new LED technology was developed using GaN substrates, generating GaN-on-GaN diodes (gallium nitride on gallium nitride) 4. The use of the GaN substrate greatly improves the light emission. These diodes can be operated at higher current densities and produce more light from a smaller area. Their short wavelength em...

Diabetic retinopathy (DR) remains a major cause of vision loss, due to macular edema, retinal ischemia and death of retinal neurons. We previously demonstrated that acute administration of glibenclamide into the vitreous, or given orally at a non-hypoglycemic dose, protected the structure and the function of the retina in three animal models that each mimic aspects of diabetic retinopathy in humans. In this pilot study, we investigated whether one year of chronic oral glibenclamide, in a non-hypoglycemic regimen (Amglidia®, 0.4 mg/kg, Ammtek/Nordic Pharma, 5 d/week), could alleviate the retinopathy that develops in the Goto-Kakizaki (GK) rat. In vivo, retinal function was assessed by electroretinography (ERG), retinal thickness by optical coherence tomography (OCT) and retinal perfusion by fluorescein and indocyanin green angiographies. The integrity of the retinal pigment epithelium (RPE) that constitutes the outer retinal barrier was evaluated by quantitative analysis of the RPE morphology on flat-mounted fundus ex vivo. Oral glibenclamide did not significantly reduce the Hb1Ac levels but still improved retinal function, as witnessed by the reduction in scotopic implicit times, limited diabetes-induced neuroretinal thickening and the extension of ischemic areas, and it improved the capillary coverage. These results indicate that low doses of oral glibenclamide could still be beneficial for the prevention of type 2 diabetic retinopathy. Whether the retinas ofpatients treated specifically with glibenclamideare less at risk of developing diabetic complications remains to be demonstrated.