Carotenoids and Antioxidants in Age-Related Maculopathy Italian Study. Multifocal Electroretinogram Modifications after 1 Year

Fondazione G. B. Bietti-Istituto di Ricovero e Cura a Carattere Scientifico, Roma, Italy.
Ophthalmology (Impact Factor: 6.17). 02/2008; 115(2):324-333.e2. DOI: 10.1016/j.ophtha.2007.05.029
Source: PubMed

ABSTRACT To evaluate the influence of short-term carotenoid and antioxidant supplementation on retinal function in nonadvanced age-related macular degeneration (AMD).
Randomized controlled trial.
Twenty-seven patients with nonadvanced AMD and visual acuity > or =0.2 logarithm of the minimum angle of resolution were enrolled and randomly divided into 2 age-similar groups: 15 patients had oral supplementation of vitamin C (180 mg), vitamin E (30 mg), zinc (22.5 mg), copper (1 mg), lutein (10 mg), zeaxanthin (1 mg), and astaxanthin (4 mg) (AZYR SIFI, Catania, Italy) daily for 12 months (treated AMD [T-AMD] group; mean age, 69.4+/-4.31 years; 15 eyes); 12 patients had no dietary supplementation during the same period (nontreated AMD [NT-AMD] group; mean age, 69.7+/-6.23 years; 12 eyes). At baseline, they were compared with 15 age-similar healthy controls.
Multifocal electroretinograms in response to 61 M-stimuli presented to the central 20 degrees of the visual field were assessed in pretreatment (baseline) conditions and, in nonadvanced AMD patients, after 6 and 12 months.
Multifocal electroretinogram response amplitude densities (RAD, nanovolt/deg(2)) of the N1-P1 component of first-order binary kernels measured from 5 retinal eccentricity areas between the fovea and midperiphery: 0 degrees to 2.5 degrees (R1), 2.5 degrees to 5 degrees (R2), 5 degrees to 10 degrees (R3), 10 degrees to 15 degrees (R4), and 15 degrees to 20 degrees (R5).
At baseline, we observed highly significant reductions of N1-P1 RADs of R1 and R2 in T-AMD and NT-AMD patients when compared with healthy controls (1-way analysis of variance P<0.01). N1-P1 RADs of R3-R5 observed in T-AMD and NT-AMD were not significantly different (P>0.05) from controls. No significant differences (P>0.05) were observed in N1-P1 RADs of R1-R5 between T-AMD and NT-AMD at baseline. After 6 and 12 months of treatment, T-AMD eyes showed highly significant increases in N1-P1 RADs of R1 and R2 (P<0.01), whereas no significant (P>0.05) change was observed in N1-P1 RADs of R3-R5. No significant (P>0.05) changes were found in N1-P1 RADs of R1-R5 in NT-AMD eyes.
In nonadvanced AMD eyes, a selective dysfunction in the central retina (0 degrees -5 degrees ) can be improved by the supplementation with carotenoids and antioxidants. No functional changes are present in the more peripheral (5 degrees -20 degrees ) retinal areas.

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Available from: Vincenzo Parisi, Apr 21, 2014
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    • "To our knowledge, this is the first longitudinal study, based on an objective electrophysiological technique, documenting the long-term effects of Saffron antioxidant on retinal function in AMD. While several other studies have already shown significant effects of antioxidant supplementation on retinal function [8] [10] [13], all these previous studies were more limited either in their follow-up duration or in the number of testing sessions. The current data show that changes in fERG threshold (and consequently its reciprocal value sensitivity) after supplementation were within-session consistent, reproducible , and durable over a 15-month follow-up period. "
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    ABSTRACT: Objectives. In a previous randomized clinical trial (Falsini et al. (2010)), it was shown that short-term Saffron supplementation improves retinal flicker sensitivity in early age-related macular degeneration (AMD). The aim of this study was to evaluate whether the observed functional benefits from Saffron supplementation may extend over a longer follow-up duration. Design. Longitudinal, interventional open-label study. Setting. Outpatient ophthalmology setting. Participants. Twenty-nine early AMD patients (age range: 55-85 years) with a baseline visual acuity >0.3. Intervention. Saffron oral supplementation (20 mg/day) over an average period of treatment of 14 (±2) months. Measurements. Clinical examination and focal-electroretinogram-(fERG-) derived macular (18°) flicker sensitivity estimate (Falsini et al. (2010)) every three months over a followup of 14 (±2) months. Retinal sensitivity, the reciprocal value of the estimated fERG amplitude threshold, was the main outcome measure. Results. After three months of supplementation, mean fERG sensitivity improved by 0.3 log units compared to baseline values (P < 0.01), and mean visual acuity improved by two Snellen lines compared to baseline values (0.75 to 0.9, P < 0.01). These changes remained stable over the follow-up period. Conclusion. These results indicate that in early AMD Saffron supplementation induces macular function improvements from baseline that are extended over a long-term followup.
    Evidence-based Complementary and Alternative Medicine 07/2012; 2012:429124. DOI:10.1155/2012/429124 · 1.88 Impact Factor
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    • "Adaptation to changes in oxidative environments is critical for the survival of retina and RPE cells. Clinical trials demonstrated a significant reduction toward retinal degeneration upon intake of antioxidants such as lutein, zeaxanthin, zinc, vitamin C, and vitamin E [6] [7]. Oxidation of polyunsaturated fatty acids (PFA) and abundant photosensitizers in the RPE induce generation of reactive oxygen species (ROS) upon exposure to visible light [8] [9]. "
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    ABSTRACT: The retinal pigment epithelium (RPE) is essential for retinoid recycling and phagocytosis of photoreceptors. Understanding of proteome changes that mediate oxidative stress-induced degeneration of RPE cells may provide further insight into the molecular mechanisms of retinal diseases. In the current study, comparative proteomics has been applied to investigate global changes of RPE proteins under oxidative stress. Proteomic techniques, including 2D SDS-PAGE, differential gel electrophoresis (DIGE), and tandem time-of-flight (TOF-TOF) mass spectrometry, were used to identify early protein markers of oxidative stress in the RPE. Two biological models of RPE cells revealed several differentially expressed proteins that are involved in key cellular processes such as energy metabolism, protein folding, redox homeostasis, cell differentiation, and retinoid metabolism. Our results provide a new perspective on early signaling molecules of redox imbalance in the RPE and putative therapeutic target proteins of RPE diseases caused by oxidative stress.
    Journal of proteomics 11/2010; 74(2):254-61. DOI:10.1016/j.jprot.2010.11.004 · 3.93 Impact Factor
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    • "RGC death may occur via a variety of mechanisms involving, for example, reactive oxygen species (ROS) (Bonne et al 1998), excitatory amino acids (Dreyer 1998), nitric oxide (Neufeld 1999) and apoptosis (McKinnon 1997). Previous studies on the protective effects of carotenoids (including astaxanthin) against retinal damage have primarily focused on age-related maculopathy (Parisi et al 2008). Moreover, to our knowledge no examination has been made of the in-vitro neuroprotective effects of astaxanthin against oxidative stress using retinal ganglion cells or in-vivo models of retinal damage. "
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    ABSTRACT: We have investigated whether astaxanthin exerted neuroprotective effects in retinal ganglion cells in-vitro and in-vivo. In-vitro, retinal damage was induced by 24-h hydrogen peroxide (H2O2) exposure or serum deprivation, and cell viability was measured using a WST assay. In cultured retinal ganglion cells (RGC-5, a rat ganglion cell-line transformed using E1A virus), astaxanthin inhibited the neurotoxicity induced by H2O2 or serum deprivation, and reduced the intracellular oxidation induced by various reactive oxygen species (ROS). Furthermore, astaxanthin decreased the radical generation induced by serum deprivation in RGC-5. In mice in-vivo, astaxanthin (100 mg kg(-1), p.o., four times) reduced the retinal damage (a decrease in retinal ganglion cells and in thickness of inner plexiform layer) induced by intravitreal N-methyl-D-aspartate (NMDA) injection. Furthermore, astaxanthin reduced the expressions of 4-hydroxy-2-nonenal (4-HNE)-modified protein (indicator of lipid peroxidation) and 8-hydroxy-deoxyguanosine (8-OHdG; indicator of oxidative DNA damage). These findings indicated that astaxanthin had neuroprotective effects against retinal damage in-vitro and in-vivo, and that its protective effects may have been partly mediated via its antioxidant effects.
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