Measurement of Carotenoids in Perifovea using the Macular Pigment Reflectometer.

The macular pigment reflectometer (MPR) objectively measures the overall macular pigment optical density (MPOD) and further provides the lutein optical density (L-OD) and zeaxanthin optical density (Z-OD) in the central 1 degree of the fovea. A modification of the technique was developed to evaluate in vivo carotenoid density eccentric to the fovea. An adjustable track system with red LED lights was placed 6.1 m away from the participant to facilitate ocular fixation. Lights were spaced appropriately to create increments of 1 degree retinal disparity during the reflectometry measurements. All reflectometry measurements were obtained with pupillary dilation. The mean MPR-MPOD value for the central measurement was 0.593 (SD 0.161) with an L-OD to Z-OD ratio of 1:2.61. The MPR-MPOD value at 1 degree was 0.248 and the mean MPR-MPOD value at 2 degrees in the parafoveal region was 0.143. The L-OD to Z-OD ratio at 1 degree and 2 degrees off center was 1.38:1.0 and 2.08:1.0, respectively. The results demonstrate that MPOD measurements obtained using the MPR decrease as a function of retinal eccentricity and that there is a higher concentration of zeaxanthin centrally compared to lutein. The L-OD to Z-OD ratio changes with foveal eccentricity, with twice more lutein than zeaxanthin at 2 degrees off center. Our technique successfully provides a quick in vivo method for the measurement of macular pigment optical density at various foveal eccentricities. The results agree with prior published in vivo and in vitro xanthophyll carotenoid density distribution measurements.

Effects of Zeaxanthin on Growth and Invasion of Human Uveal Melanoma in Nude Mouse Model.

Uveal melanoma cells were inoculated into the choroid of nude mice and treated with or without intraocular injection of zeaxanthin. After 21 days, mice were sacrificed and the eyes enucleated. Histopathological analysis was performed in hematoxylin and eosin stained frozen sections. Melanoma developed rapidly in the control group (without treatment of zeaxanthin). Tumor-bearing eye mass and tumor mass in the control group were significantly greater than those in zeaxanthin treated group. Melanoma in the controlled eyes occupied a large part of the eye, was epithelioid in morphology, and was with numerous mitotic figures. Scleral perforation and extraocular extension were observed in half of the eyes. Melanomas in zeaxanthin treated eyes were significantly smaller with many necrosis and apoptosis areas and no extraocular extension could be found. Quantitative image analysis revealed that the tumor size was reduced by 56% in eyes treated with low dosages of zeaxanthin and 92% in eyes treatment with high dosages of zeaxanthin, as compared to the controls. This study demonstrated that zeaxanthin significantly inhibits the growth and invasion of human uveal melanoma in nude mice, suggesting that zeaxanthin may be a promising agent to be explored for the prevention and treatment of uveal melanoma.

Beneficial effect of zeaxanthin on retinal metabolic abnormalities in diabetic rats.

PURPOSE: Oxidative damage and growth factors are implicated in the pathogenesis of retinopathy in diabetes. Recent studies have shown that two dietary carotenoids, lutein and zeaxanthin (Zx), that are specifically concentrated within ocular tissues, may play important roles in maintaining their integrity. This study is to evaluate the potential protective effects of Zx against retinal oxidative damage and growth factors in diabetes. METHODS: A group of rats received normal powdered diet or powdered diet supplemented with 0.02% or 0.1% Zx soon after induction of diabetes. Age-matched normal rats served as control subjects. At 2 months of diabetes, oxidative stress, vascular endothelial cell growth factor (VEGF), and intercellular adhesion molecule (ICAM)-1 were quantified in the retina. RESULTS: Zx supplementation prevented diabetes-induced increase in retinal damage, and increases in VEGF and ICAM-1. The levels of lipid peroxide, oxidatively modified DNA, electron transport complex III, nitrotyrosine, and mitochondrial superoxide dismutase were similar in the retinas of Zx-treated diabetic rats and normal control rats, and these values were significantly different from those obtained from diabetic rats without any supplementation. In the same rats, Zx also prevented diabetes-induced increases in retinal VEGF and ICAM-1. Both 0.02% and 0.1% Zx had similar effects on diabetes-induced retinal abnormalities, and these effects were achieved without ameliorating the severity of hyperglycemia. However, Zx administration failed to prevent a diabetes-induced decrease in retinal GSH levels. CONCLUSIONS: Zx significantly inhibits diabetes-induced retinal oxidative damage and elevation in VEGF and adhesion molecule, all abnormalities that are associated with the pathogenesis of diabetic retinopathy. The results suggest that Zx supplementation has the potential to inhibit the development of retinopathy in diabetic patients.