The effect of a high dose lutein/zeaxanthin supplement on macular pigment optical density (MPOD) and skin carotenoid (SC) levels in healthy subjects was investigated. This is a prospective, single-arm, open-label study. Subjects were 16 Japanese, age 26-57 years. Subjects took a supplement containing 20 mg/day of lutein, 4 mg/day of zeaxanthin, and other antioxidants (vitamin C, vitamin E, zinc, copper) for 16 weeks. MPOD levels were measured by a two-wavelength autofluorescence imaging technique. SC levels were measured by reflection spectroscopy. Total volume of MPOD within 9° eccentricity significantly increased by week 8 and continued to increase until week 16 (p < 0.0001, two-way factorial ANOVA). The increase rate of MPOD was significantly higher in subjects with body mass index (BMI) less than 25 kg/m 2 (n = 13) compared to those of 25 kg/m 2 and higher (n = 3). SC levels increased significantly by week 4 and continued to increase until week 16 (p < 0.0001, two-way factorial ANOVA). All subjects completed the study without any serious adverse events. These results demonstrated the effectiveness of a high dose lutein/zeaxanthin supplement for MPOD volume and SC levels without serious adverse events. The human macula contains yellow pigment, called macular pigment (MP), consisting of three carotenoids, lutein ((3R, 3′R, 6′R)-lutein), zeaxanthin ((3R, 3′R)-zeaxanthin), and meso-zeaxanthin ((3R, 3′S; meso)-zeaxanthin) 1,2. MP absorbs blue light and acts as a filter that may attenuate photochemical damage to the retina due to blue light exposure and potentially protects against light-induced oxidative damage in the retina by quenching oxygen radicals 3-5. MP functions to improve contrast sensitivity and reduces night glare 6-9. Some studies have reported that MP optical density (MPOD) levels in eyes with age-related macular degeneration (AMD) are significantly lower than those in normal, healthy eyes 10,11. The light protection effect of MP is thought to prevent age-related macular degeneration (AMD) 7,12-15 , and our previous study on a Japanese population indicated that lower MPOD levels may be a risk factor for AMD progression 16. Carotenoids such as lycopene, alpha-. beta-, gamma-, delta-carotene, beta-cryptoxanthin, lutein, and zeaxanthin are contained in the epidermis, dermis, and subcutaneous fat 17. These carotenoids protect skin against oxidation induced by sunlight exposure. Lutein and zeaxanthin have been reported to reduce lipid peroxidation and increase moisture in the skin 18. The anti-oxidative effect of lutein also protects against UV-induced skin damage 19. Regarding the subset of carotenoids found in the human macula, previous studies have reported a weak to moderate correlation between MPOD and skin carotenoid (SC) levels measured by resonance Raman spectroscopy (RRS) 20-23. The Age-related Eye Disease Study (AREDS) Research Group conducted the first multi-center, randomized trial to verify the prophylactic effect of a supplement containing vitamin C, vitamin E, beta-carotene, and zinc, and d...

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Effects of oil-droplet size, the weight ratio of oil to wall material and the storage temperature on the oxidation of methyl linoleate microencapsulated with maltodextrin by spray-drying were examined. The oxidation of methyl linoleate was more retarded for the microcapsules prepared from the emulsion having smaller oil droplets. The oxidation was more suppressed for the microcapsules having a lower weight ratio of oil to wall material. The fraction of unoxidized methyl linoleate leveled off after 10-to 15-days storage. The level, Y ∞ , depended on the weight ratio. The dependence of Y ∞ on the weight ratio was analyzed based on the percolation theory, and the three-dimensional model of the theory was suitable to express the dependence. The effect of the storage temperature on the oxidation of microencapsulated methyl linoleate was also examined, and the activation energy was evaluated. The value of the energy suggested that the oxidation itself was a rate-limiting step for the oxidation of methyl linoleate encapsulated with maltodextrin.

The hydrolysis kinetics of trisaccharides consisting of glucose, galactose, and fructose residues with different glycosidic bonds, 1-kestose, d-melezitose, d-raffinose, and lactosucrose, in subcritical water were conducted over the temperature range of 150-230 degrees C and at a constant pressure of 10 MPa. The hydrolysis of trisaccharides in subcritical water proceeded consecutively, i.e., one cleavage of the two bonds antedated the other. The preceding cleavage was not expressed by the first-order kinetics, but by the kinetics considering the concentration of the acidic compounds, which were produced by the degradation of the constituent monosaccharides. The hydrolysis of the constituent disaccharides, except sucrose composed of the alpha-Glc-(1-->2)-beta-Fru bond, obeyed first-order kinetics. All of the rate constants of the hydrolytic kinetics were determined, and the values were found to depend on the type of bond.

Purpose To observe the macular pigment (MP) appearances in eyes with macular hole (MH) and clarify the origin of the appearances. The mechanisms underlying the development of MH are discussed based on the observation of MP. Methods This observational case series included 33 eyes of 31 patients with MH who underwent vitrectomy. The MP optical density was measured using the two-wavelength fundus autofluorescence technique. The exact localization of MP was evaluated by comparing MP distribution images and optical coherent tomography B-scan images. Results MP was missing at the MH. The area of the MP defect corresponded with the area of the defect of outer plexiform layer. MP was present in the retinal flap in stage 2 MH that included glia (Müller cells) and plexiform layers and in the operculum in stage 3 MH, which mainly comprised Müller cells. Cystic spaces in the outer plexiform layer surrounding stage 3 and 4 MHs showed a honeycomb appearance on MP images. MP reappeared to form an irregularly shaped pigment plane after surgical closure of MH. The MP optical volume did not change before and after surgery. Fellow eyes with a central dip in MP distribution subsequently developed MH. Conclusions The characteristic appearances of MP at the MH were attributed to MP in the plexiform layers and Müller cell cones. A central dip of MP distribution might be a sign of Müller cell cone damage that proceeds with MH formation. Translational Relevance Observation of MP was useful for understanding the mechanisms of MH formation.