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Schierz, C. IS LIGHT WITH LACK OF RED SPECTRAL COMPONENTS A RISK FACTOR FOR AGE-RELATED... organelles which are responsible for the cell’s energy and metabolism regulation. The photoacceptor for red light and near IR radiation is the enzyme “cytochrome c oxidase” (COX). It is part of the respiratory chain which is located in the inner membrane of RPE- mitochondria. This electron transport chain acts as radical scavenger and counteracts oxidative stress. Action spectra with four maxima at 620 nm, 675 nm, 760 nm, and 830 nm are presented by Karu, and Kolyakov (2005). One of them is shown in Figure 3 as 5. To sum up the validity of PBM, the conclusion of Geneva (2016) can be quoted: “Given the promising pre-clinical results and the equally promising first few translations to human patients, we should expect a growth in the field of photobiomodulation applied to treat common retinal conditions such as age-related macular degeneration...” Table 1 – Studies about light treatments of the retina by means of photobiomodulation (PBM). References Albarracin et al. (2011) Albarracin et al. (2013) Qu et al. (2010) Di Marco et al. (2014) Natoli et al. (2010) Olmo- Aguado et al. (2016) Begum et al. (2013) Fuma et al. (2015) Species 54 albino rats 60 albino rats 8 groups of albino rats 44 albino rats 24 albino rats 62 Wistar rats 29 mice Cultured human RPE-cells Spectrum Intensity Light treatment Exposure time 3 min, daily at 9 AM, for 5 consecutive days 3 min, daily at 9 AM, for 5 consecutive days 30 min, 3 h before, and 0, 24 and 48 h after LD 3 min for 7 days 3 min, daily at 9 AM, for 5 days 1h 24 h 6 min, daily at 6AM and 6PM, for 14 days 250 s for 4 days, twice per day Treatment effect Attenuation of histopathologic alterations Increased stability of photoreceptors in cond. of oxidative stress Protects retinal cells against light-induced damage Reduction of cell death Normalisation of gene expression which was reduced by LD Attenuation of insults due to raised intra- ocular pressure (IOP) Increase in cytochrome c oxidase (COX) Reduction of reactive oxygen species production Remarks Light damage: 24 h with 18 W cool white FL, 1000 lx at bottom of cage Receptor damage: Rats placed in hyperoxic environment (75% oxygen) Light damage (LD): 3 h of 1800 lx and 2700 lx, respectively. Light damage before treatment: 24 h with FL, 1000 lux. Light damage before treatment: 24 h with FL, 1000 lux. Induction of experimental ischaemia by increasing IOP for 60 min. Aged mice, at room illumination of 50 lx. Additional effect: Enhancement of phagocytic activity. 670 nm, LED 670 nm LED 670 nm LED 670 nm LED 670 nm LED 630 nm LED 670 nm LED 670 nm LED 600 W/m2 600 W/m2 50 mW (?) 250-300 W/m2 600 W/m2 16,5 W/m2, 5,5 W/m2 19 W/m2 38,9 W/m2 Chu-Tan et al. (2016) 55 albino rats 670 nm LED 600 W/m2 5 days at 9AM for: 3 min, 6 min, 12 min, or 30 min Increased prevention of cell death (assessed by DNA fragmentation) After treatment: 24 h exposure to 750 lx, 1000 lx, or 1500 lx light from cold-white FL Ivandic et al. (2008) 203 AMD patients 780 nm semi- conductor laser diode 75 W/m2 40 s, four treatments (two treatments per week) Improvement in visual acuity, reduction of edema, bleeding, dis- torted vision, scotoma, and colour blindness Application: Transconjunc- tivally to the macula Merry et al. (2017) 42 human eyes with dry AMD 590 nm + 670 nm + 790 nm LEDs 670 nm: 500–800 W/m2 670 nm: 88 s Improvement in visual acuity and contrast sensitivity, reduction in drusen volume 590 nm at 4 mW (?), and 670 nm at 0,6 mW (?) for 35 s, with 2,5 Hz, 250 ms on,150 ms off. Rodriguez- Santana et al. (2008) 1 AMD patient 904 nm pulsed laser 45 kJ/m2/day (?) Fractioned daily radiant exposure Several positive clinical outcomes (e.g. visual acuity, ocular fundes, intraocular pressure...) Note: Time schedule and application method is unclear Proceedings of 29th CIE Session 2019 117PDF Image | LIGHT WITH LACK OF RED SPECTRAL COMPONENTS v amd
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