Abstract
Using in vivo adaptive optics (AO) scanning laser ophthalmoscopy (SLO) equipped with fluorescence imaging capabilities, we previously reported1, in the macaque retina, an immediate decrease in RPE autofluorescence (568nm excitation; 624Δ40nm emission) intensity in response to 568nm light, followed by either full recovery or permanent retinal damage. Here, we explored the effect of 488nm light exposures on the intensity of autofluorescence and long term retinal health. Using the fluorescence-AOSLO, macaques were simultaneously exposed to a small amount of near IR and 488nm light of various powers for 15 minutes over a square ½° field. Pre- and post-exposure images were taken in a 2° field. For exposures of 15 J/cm2 or greater, long term disruption of the RPE was observed within 2 weeks. Immediately following the 488nm exposures, a significant decrease in autofluorescence intensity was observed when using 488nm light for autofluorescence excitation. The magnitude of this decrease was comparable to the previously reported 568nm autofluorescence decrease observed following 568nm exposures of similar retinal irradiance. Interestingly, only a minor decrease in autofluorescence intensity was observed following the 488nm exposures when 568nm light was used for excitation. These results suggest that different lipofuscin fluorophores are affected by the 488nm and 568nm exposures. This also may indicate that the decrease in autofluorescence is caused by a quenching or bleaching mechanism. Future work is needed to identify the molecular mechanisms involved. Regardless, long-term damage was observed following exposures that were an order of magnitude below previously reported photochemical damage thresholds for 488nm2. Thus, the ANSI Standard and other safety guidelines again appear to provide insufficient protection from photochemical damage.
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