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J. T. Eells, S. Gopalakrishnan, B. Abroe, R. Albarracin, K. Valter-Kocsi; 670 nm Photobiomodulation Attenuates Light-Induced Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2263.
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Irradiation by light in the far-red to near-infrared (NIR) region of the spectrum (photobiomodulation; PBM) has been demonstrated to attenuate the severity of degenerative retinal diseases in experimental and clinical studies. The cytoprotective actions of NIR-PBM have been attributed to improved mitochondrial energy production and the upregulation of cytoprotective factors. The purpose of this study was to test the hypothesis that a brief course of 670 nm photobiomodulation would protect against the loss of retinal function, prevent mitochondrial dysfunction and attenuate photoreceptor loss in the light damaged retina.
The eyes of adult female Sprague Dawley rats (250 g) were treated with 670 nm light for 90 sec at 50 mW/cm2 (fluence = 4.5 joules/cm2 ) using a light emitting diode array (Quantum Devices, Inc). Rats were treated once per day for 5 days prior to light damage [LD] (1500 lux for 24 h). Sham-treated LD rats were restrained for 90 sec, but not exposed to 670 nm PBM. At day 7 following LD, retinal function was examined by ERG. At day 14, eyes were enucleated. One eye was prepared for histological evaluation and the retina from the other eye was removed, snap frozen and stored at -80 C for future analysis of mitochondrial function and antioxidant concentrations.
670 nm photobiomodulation protected against LD-induced loss of rod and cone function. In sham-treated LD animals rod-mediated b-wave amplitude was 320 + 78 µV compared to 450 + 65 µV in NIR-treated LD rats. The rod-mediated b/a ratio was 14 + 4 in sham-treated LD animals and 22 + 6 in NIR-treated LD animals (p < 0.05). The cone-mediated b-wave in LD rats was 103 + 9 µV compared to 165 + 25 µV (p < 0.05) in NIR-treated LD rats.
Previous studies in our laboratory have demonstrated neuroprotective and retinoprotective actions of 670 nm PBM light treatment in vitro and in vivo. The present study extends these findings to include protection against light-damage induced photoreceptor dysfunction. Given the reliance of photoreceptors on mitochondrial oxidative metabolism and the evidence for LD-induced mitochondrial injury, we speculate that the observed retinoprotective actions of NIR PBM are due, in part, to the prevention of photoreceptor mitochondrial dysfunction and the induction of mitochondrial repair in retinal light damage.
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