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C.E. Reme, C. Grimm, M.I. Simon, A. Wenzel; Effects of Blue- and Green Light in Arrestin / Rhodopsinkinase Double Knock Out (Arr-/- / RK -/-) Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):5132.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Previous studies in rats revealed strong photoreceptor susceptibility to blue light damage, possibly due to a rhodopsin - like photoproduct, generated from activated rhodopsin by blue light, enabling a large number of photon absorptions per time. We investigated in Arr-/- / RK -/- mice whether lack of rhodopsin inactivation increases photoregeneration and lesions after blue light exposure. Methods: Arr -/- / RK -/- mice and wildtype controls were raised in total darkness, further wildtype controls were raised in an LD cycle. 5- 8 week mice were exposed to blue light (403 +/- 10 nm) or green light (550 +/- 10 nm) for varying time periods, sacrificed 3 days after exposure for morphological evaluation and 6 h after exposure for AP1 analysis. Photoregeneration of rhodopsin was measured by exposing mice to 1 min of green immediately followed by 2 min of blue. Rhodopsin levels were determined in isolated retinas. Results: In all groups, a distinct lesion appeared after 1 min of exposure to blue light of 30 mW/cm2. With increasing exposure durations, the damaged area extendet. Abundant apoptotic photoreceptor cells and macrophages were prominent. Tunel staining verified apoptosis. In contrast to blue light exposed specimens, green light did not induce any morphologically apparent lesions. However, the transcription factor AP1, a key component in light-induced apoptosis, was upregulated in blue as well as green light exposed retinas. Exposure for 1 min to green bleached 90% of rhodopsin, when this was immediately followed by 2 min of blue, 20 – 40 % of a rhodopsin - like photoproduct with 500 nm absorption peak was measured.Conclusion: The lack of rhodopsin inactivation in Arr -/-/ RK -/- mice does not increase susceptibility to blue light lesions, since all three goups of mice were damaged after 1 min of exposure. Despite an induction of AP1after green light, no apoptosis was induced. Apparently, no death cascade is initiated through AP1 under this condition. Alternatively, a to date unknown mechanism inhibits the execution of apoptosis downstream of AP1. We cannot exclude the possibility that blue light lesions too are independent of AP1 induction. Different apoptotic signals may operate such as photoproducts specific for blue light.
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