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(Investigative Ophthalmology and Visual Science. 2002;43:3538-3549.)
© 2002 by The Association for Research in Vision and Ophthalmology, Inc.

Elevated Retinal Zeaxanthin and Prevention of Light-Induced Photoreceptor Cell Death in Quail

Lauren R. Thomson1,2,3,4, Yoko Toyoda1,2,4,5, Andrea Langner1,2,6, Francois C. Delori1,2, Kevin M. Garnett7,8, Neal Craft9, Cathleen R. Nichols10, Kimberly M. Cheng10 and C. Kathleen Dorey1,2

1 From the Schepens Eye Research Institute and 2 Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; 3 Columbia University School of Medicine, New York, New York; the 6 Department of Ophthalmology, University Eye Clinic, Leipzig, Germany; 7 Applied Food Biotechnology Inc., O’Fallon, Missouri; 9 Craft Technologies, Inc., Wilson, North Carolina; and the 10 Department of Animal Sciences, University of British Columbia, Vancouver, British Columbia, Canada.

PURPOSE. Inferential evidence indicates that macular pigments (lutein and zeaxanthin) protect photoreceptors and/or retard age-related macular degeneration. These experiments tested the hypothesis that retinal zeaxanthin prevents light-induced photoreceptor cell death.

METHODS. Retinal damage was assessed in quail fed a carotenoid-deficient (C-) diet for 6 months. Groups of 16 birds (8 male, 8 female) were fed a C- diet supplemented with 35 mg 3R,3'R-zeaxanthin for 1, 3, or 7 days; one group was continued on C- diets. Half of each group was exposed to intermittent 3200-lux white light (10 1-hour intervals separated by 2 hours in dark). After 14 additional hours in the dark, one retina of each quail was collected for HPLC analysis, and the contralateral retina was embedded in paraffin for counts of apoptotic nuclei.

RESULTS. After 7 days’ supplementation, concentrations of zeaxanthin in serum, liver, and fat had increased by factors of 50.8, 43.2, and 6.5, respectively (all P < 0.001). In contrast, retinal zeaxanthin fluctuated significantly upward on day 3, but there was no net change on day 7. The number of apoptotic rods and cones in light-damaged eyes correlated significantly and inversely with zeaxanthin concentration in the contralateral retina (r = -0.61; P < 0.0001 and r = -0.54; P < 0.002), but not with serum zeaxanthin. Similar correlations were observed with retinal lutein, which correlated strongly with retinal zeaxanthin (r = 0.95; P < 0.0001).

CONCLUSIONS. Retinal zeaxanthin dose dependently reduced light-induced photoreceptor apoptosis; elevated serum levels did not. These data provide the first experimental evidence that xanthophyll carotenoids protect photoreceptors in vivo.




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