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Minzhong Yu, Craig Beight; Lutein and zeaxanthin isomers protect photoreceptors against blue light-induced degeneration. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5916. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Oxidative stress and endoplasmic reticulum stress are major factors underlying photoreceptor degeneration. Lutein and zeaxanthin isomers (L/Zi), consisting of lutein, zeaxanthin and mesozeaxanthin carotenoids, are found widely in many foods and protect against cell damage by ameliorating oxidative stress in retina. In this study, we examined the effect of L/Zi supplementation in a mouse model of light-induced photoreceptor degeneration.
L/Zi (10 mg/kg) dissolved in sunflower oil (SFO, 1 mg/ml) or equal volume of SFO as vehicle was administered by daily oral gavage to 2-month old BALBc/J mice in treatment group (n=7) and vehicle group (n=7), respectively for a 5 day period. On Day 2, animals were exposed for 1 hour to blue light (5,000 lux) obtained by filtering white fluorescent light by a filter which transmitted light between 380 and 570 nm (Midnight Blue 5940, Solar Graphics, Clearwater, FL). ERG was tested to show the functional change of retina. Nrf2 and GRP78 were tested by western blot.
ERG amplitudes were significantly reduced in the vehicle control mice after light exposure as compared to the baseline collected before the light exposure. ERG amplitudes after light exposure were significantly higher in the L/Zi treated group than in the vehicle control group. These ERG amplitudes were lower than baseline, indicating incomplete protection. In light-exposed retinas, Nrf2 was upregulated and GRP78 was downregulated by L/Zi treatment.
Treatment with L/Zi can protect photoreceptors against degeneration induced by high intensity blue light. This treatment effect is probably related to the decrease of oxidative stress and endoplasmic reticulum stress by the L/Zi treatment. Future studies will examine the potential for L/Zi in inherited forms of photoreceptor degeneration involving oxidative stress.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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