Low Light Damage as a Model of Retinal Degeneration in Rats

BENEDETTO, MARIA MERCEDES; QUINTEROS QUINTANA, MARIA LUZ; GUIDO, MARIO EDUARDO; CONTIN, MARIA ANA

Córdoba

Congreso; 16th International Congress on Photobiology; 2014

International Union of Photobiology

The retina is part of the central nervous system[1], adapted to capture light photons and transmit the information to brain. In mammals, light fulfill two important role; visual function through rods and cones photoreceptor, and synchronization of circadian rhythms to a 24h solar cycle through a subpopulation of photosensitive retinal ganglion cells. However, the excess of light stimuli may cause retinal degeneration or accelerate genetic retinal diseases[2]. There are numerous papers published that evaluate the effects of bright light exposure on retinal morphophysiology, however the process of retinal cell death by low intensity light stress may be different and it is not well characterized yet. To evaluate the effects of constant exposure to low intensity light on the retina; 3 months age Wistar albino rats were constantly exposed to cool white light of 200 lux intensity 1 to 7 days. Control animals were exposed to cycles of light (200 lux)/dark (0 lux) of 12hs/12hs or constant darkness. We found that constant light, but not cyclic exposure, produce a reduction in outer nuclear layer thickness. We revealed that photoreceptors die by a caspase-3 independent mechanism and rhodopsin expression was not alterated; nevertheless it was more phosphorylated in ser334 in relation to control animals[3]. In this work, we investigate if oxidative stress mechanisms are involved and we found evidence of oxidative stress by catalase activity and lipid peroxidation. To asses photoreceptor cells function ERGs were performed and we observed alterations in scotopic a-wave amplitude and latency time.