Prevention Of Age-related Macular Degeneration Research Articles

Protective effect of lutein on ARPE-19 cells upon H2O2-induced G2/M arrest.

Oxidative damage is a key factor for the pathogenesis of age‑related macular degeneration (AMD), therefore, anti-oxidative stress is a valuable method for the prevention or treatment of AMD. The aim of the present study was to reveal the protective mechanism of lutein on retinal pigment epithelium (RPE) cells subjected to oxidative stress. Acute retinal pigment epithelial 19 (ARPE‑19) cells were exposed to oxidative stress induced by H2O2 following lutein pretreatment. The activities of caspases, level of intracellular reactive oxygen species (ROS) and cell cycle were analyzed using flow cytometry. The expression levels of cell cycle regulatory proteins and inflammation‑associated genes were detected using western blot and reverse transcription‑polymerase chain reaction analyses, respectively. The data showed that oxidative stress reduced cell viability, and increased total apoptosis and ROS generation, however, lutein prevented cells from oxidative stress‑induced damage. In addition, oxidative damage triggered G2/M phase arrest of the ARPE‑19 cells, which was reversed by lutein in a concentration‑dependent manner, through the activation of cyclin‑dependent kinase1 and cell division cycle 25C, and degradation of cyclin B1. These results demonstrated that lutein may be an effective antioxidant, which can be applied in the prevention of AMD, or other age-related diseases associated with oxidative damage.

Prevention of Age-Related Macular Degeneration.

Age-related macular degeneration (AMD) compromises quality of life. However, the available therapeutic options are limited. This has led to the identification of modifiable risk factors to prevent the development or alter the natural course and prognosis of AMD. The identification and modification of risk factors has the potential for greater public health impact on reducing morbidity from AMD. Likewise, identifying the imaging clues and genetic clues could serve as a guide to recognizing the propensity for progression to severe and end stages of the disease. Several attempts, both successful and unsuccessful, have been made for interventions that could delay the progression of AMD. Of these, pharmacological interventions have shown promising results. The Age-Related Eye Disease Study 1 and 2 have shown the beneficial role of antioxidants in a selected group of patients.

NADPH Oxidase Activity in Retinal Pigmented Epithelium as a Target for Prevention of Age-related Macular Degeneration

Considerable evidence points to macular oxidative stress as a key driver of age-related macular degeneration (AMD). In particular, retinal pigmented epithelial (RPE) cells subjected to oxidative stress are prone to apoptosis or senescence; lose their tight junctions; decrease their production of factors which provide trophic support for retinal photoreceptors, suppress choroidal neovascularization, and control complement activation; and boost their production of vascular endothelial growth factor (VEGF), a major stimulant to neovascularization – all effects which are consistent with the pathogenesis of AMD. There is good reason to suspect that NADPH oxidase activity in RPE cells is the key source of the oxidative stress that compromises RPE function in AMD. Studies with other cell lines indicate that a number of risk factors for AMD – including cigarette smoke, homocysteine, hyperglycemia, cadmium, and up-regulated activation of the alternative complement cascade – have the ability to stimulate NADPH oxidase activity, as does all-trans-retinal, a suspected pathogenic factor in AMD. Hence, measures which can down-regulate NADPH oxidase activity may have potential for preventing or controlling AMD. These may include high-dose statins – found to reverse features of early AMD in about half of patients in a recent pilot study – and spirulina, a rich source of the chromophore phycocyanobilin (PhyCB ). PhyCB is a biliverdin derivative that can mimic the intracellular physiological role of bilirubin as an NADPH oxidase inhibitor. Patients with Gilbert syndrome or relatively high plasma unconjugated bilirubin may be at lower risk for AMD owing to bilirubin’s inhibitory impact on NADPH oxidase; this prediction could be readily tested in epidemiological studies.

Prevention of Age-Related Macular Degeneration

Prevention of Age-Related Macular Degeneration

The Age-Related Eye Disease 2 Study: Micronutrients in the Treatment of Macular Degeneration.

Age-related macular degeneration (AMD) is one of the leading causes of vision loss in the elderly. With an increasingly aged population worldwide, the need for the prevention of AMD is rising. Multiple studies investigating AMD with the use of animal models and cell culture have identified oxidative stress-related retinal damage as an important contributing factor. In general, diet is an excellent source of the antioxidants, vitamins, and minerals necessary for healthy living; moreover, the general public is often receptive to recommendations made by physicians and health care workers regarding diet and supplements as a means of empowering themselves to avoid common and worrisome ailments such as AMD, which has made epidemiologists and clinicians enthusiastic about dietary intervention studies. A wide variety of nutrients, such as minerals, vitamins, ω-3 (n-3) fatty acids, and various carotenoids, have been associated with reducing the risk of AMD. Initial results from the Age-Related Eye Disease Study (AREDS) indicated that supplementation with antioxidants (β-carotene and vitamins C and E) and zinc was associated with a reduced risk of AMD progression. The AREDS2 follow-up study, designed to improve upon the earlier formulation, tested the addition of lutein, zeaxanthin, and ω-3 fatty acids. In this review, we examine the science behind the nutritional factors included in these interventional studies and the reasons for considering their inclusion to lower the rate of AMD progression.

Age-Related Macular Degeneration and Mortality in the Age-Related Eye Disease Study (AREDS): The Effect of Sex and Time

Age-related macular degeneration (AMD) shares similar risk factors and pathogeneses with cardiovascular diseases (CVDs). Epidemiologic studies over the past 2 decades analyzing the association between AMD and all-cause and CVD-specific mortality have failed to yield conclusive results. The purpose of this analysis is to investigate the sex-specific association between AMD and all-cause and CVD-specific mortality, and to assess whether duration of follow-up alters the strength of association. The database of Genotypes and Phenotypes (dbGaP) data set for the Age-Related Eye Disease Study, a randomized clinical trial of high-dose antioxidants in AMD prevention, with participants enrolled from 1992 to 1998 and followed through 2005, was used in the analysis. There were 4757 Age-Related Eye Disease Study participants aged 55 through 80 years (mean, 69.4 years; 44.1% male) recruited from 11 retinal specialty clinics. Participants had standard Age-Related Eye Disease Study AMD categories (category 1, n= 1117; category 2, n= 1062; category 3, n= 1621; category 4, n= 957). The sex-specific adjusted hazard ratio (HRadj) between baseline AMD and all-cause and CVD-specific mortality was determined at multiple time points (e.g., 5, 7, 10, and all years), adjusting for age, race, diabetes, hypertension, angina, cancer, smoking, obesity, clinical trial antioxidant treatment category, and education. Sex-specific all-cause and CVD-specific mortality. Mean follow-up was 9.6 years (range, 0.5-12.5 years), with 1087 deaths (category 1, n= 197 [17.6%]; category 2, n= 200 [18.8%]; category 3, n= 356 [22.0%]; category 4, n= 326 [34.1%]). Sex-stratified models demonstrated sex differences; in women, a significant association between AMD category 4 and all-cause mortality existed compared with category 1 at each period (HRadj, 1.5-2.3; all P ≤ 0.005); similar category 4 findings were present with CVD-specific mortality, strengthening with shorter periods (HRadj, 1.9-4.6; all P ≤ 0.01). Among men, a significant association between all AMD stages and all-cause (HRadj, 1.5-2.3; all P ≤ 0.05) and CVD-specific mortality (HRadj, 1.6-4.0; all P ≤ 0.05) existed for nearly all periods. Substantial late AMD cases and deaths exceed those in previous population-based studies to better test mortality-related hypotheses. Age-related macular degeneration was significantly associated with all-cause and CVD-specific mortality. Relationships weakened over a longer duration of follow-up, and sex seems to modify the association. Future analyses are warranted to interrogate the possible clinical usefulness of these relationships.

Resvega induces autophagy and prevents ARPE‐19 cell damage during proteasome inhibition

PurposeImpaired autophagic and proteasomal cleansing has been documented in retinal pigment epithelial (RPE) cells and age‐related macular degeneration (AMD) pathology. Omega fatty acids and resveratrol has been shown to be cytoprotective in RPE cells. We examined effects of commercial Resvega on the regulation of autophagy and cytoprotection in ARPE‐19 cells under proteasome inhibition.MethodsProtein aggregation was induced with 1 mM MG‐132 and autophagy was inhibited with bafilomycin A1. Resvega that includes vitamin C 240 mg, E 30 mg, zinc 12.5 mg, copper 1 mg, omega‐3 665 mg, lutein 10 mg, zeaxanthin 2 mg and resveratrol 30 mg was used solely and together with proteasome inhibition up to 48 h. p62 (SQSTM1), LC3 (microtubule‐associated protein 1A/1B‐light chain 3) and Hsp70 (Heat shock protein 70) were analyzed by Western blotting (WB). Tandem fluorescently tagged LC3 (GFP‐mCherry‐LC3) transfection was used to study autophagy flux in fluorescence microscopy.ResultsInhibition of proteasomes with MG‐132 upregulated Hsp70, autophagy markers p62 and LC3 detected in WB. Simultaneous treatment with MG‐132 and Resvega corresponding 25 μM resveratrol concentration highly increased amount of LC3‐II, but decreased p62 and Hsp70. Moreover, Resvega provided a clear cytoprotection under proteasome inhibition. Fluorescence microscopy showed increased autophagy flux with GFP‐mCherry‐LC3 Resvega treatment and autophagy inhibition resulted accumulation of p62 and LC3‐II.ConclusionsThis data showed how Resvega was able to induce autophagy and clear protein waste caused by proteasome inhibition in ARPE‐19 cell line. Resvega has a potential in the prevention and treatment of RPE damage and AMD.

Vascular endothelial growth factor gene polymorphisms and association with age related macular degeneration in Indian patients

BackgroundAge-related macular degeneration (AMD) is an important cause of visual impairment in elderly people. AMD is a multifactorial disease in which both environmental and genetic factors have been implicated. Various single nucleotide polymorphisms (SNPs) have been found to be associated with AMD. AimThis study was aimed to investigate the association of polymorphisms in VEGF genes with age related macular degeneration (AMD) in Indian patients. MethodGenotyping for the VEGF −1154 (G>A), −2578 (C>A), +405 (G>C) and −460 (C>T) SNPs was performed in 100 AMD patients and 100 controls by polymerase chain reaction (PCR), restriction fragment length polymorphism (PCR-RFLP) and sequencing method. ResultsOut of the four SNPs, heterozygous genotypes of VEGF −1154G>A (OR=2.58, p=0.0035), +460C>T (OR=2.90, p=0.0046), and +405G>C (OR=2.02, p=0.02) have shown susceptible association with AMD. However, VEGF −2578C>A did not show any statistical significance. Further A-A-G-T haplotype comprising of three mutant alleles revealed risk association (OR=12.7, p=0.0030) with AMD. ConclusionThe present study suggests significant genetic associations for VEGF −1154G>A, +460C>T, and +405G>C polymorphisms with AMD. Early detection of individuals with risk to these SNPs could lead to strategies for prevention, early diagnosis, and management of AMD.

All-Trans Retinoic Acid Modulates DNA Damage Response and the Expression of the VEGF-A and MKI67 Genes in ARPE-19 Cells Subjected to Oxidative Stress.

Age-related macular degeneration (AMD) is characterized by the progressive degradation of photoreceptors and retinal pigment epithelium (RPE) cells. ARPE-19 is an RPE cell line established as an in vitro model for the study of AMD pathogenesis. Oxidative stress is an AMD pathogenesis factor that induces DNA damage. Thus, the oxidative stress-mediated DNA damage response (DDR) of ARPE-19 cells can be important in AMD pathogenesis. The metabolism of retinoids—which regulates cell proliferation, differentiation, and the visual cycle in the retina—was reported to be disturbed in AMD patients. In the present work, we studied the effect of all-trans retinoic acid (ATRA, a retinoid) on DDR in ARPE-19 cells subjected to oxidative stress. We observed that ATRA increased the level of reactive oxygen species (ROS), alkali-labile sites in DNA, DNA single-strand breaks, and cell death evoked by oxidative stress. ATRA did not modulate DNA repair or the distribution of cells in cell cycle in the response of ARPE-19 cells to oxidative stress. ATRA induced autophagy in the absence of oxidative stress, but had no effect on this process in the stress. ATRA induced over-expression of proliferation marker MKI67 and neovascularization marker VEGF-A. In conclusion, ATRA increased oxidative stress in ARPE-19 cells, resulting in more lesions to their DNA and cell death. Moreover, ATRA can modulate some properties of these cells, including neovascularization, which is associated with the exudative form of AMD. Therefore, ATRA can be important in the prevention, diagnosis, and therapy of AMD.

The immunomodulatory role of retinal microglial cells in age-related macular degeneration

Age-related macular degeneration (AMD) is one of the major causes of visual impairment in the elder population. Recent studies have revealed that retinal microgliacytes may play an important role in the pathogenesis of AMD, and the activation of retinal microglia could regulate the progress of AMD. The immunomodulatory role of retinal microglial cells is reviewed in this article, so as to investigate the mechanism and provide new insight for prevention and treatment of AMD.

Vision disorders in the elderly

Visual impairment is one of the common problems in the elderly, and regular screening should be considered for early detection as well as prevention. This article describes some of the common causes of vision loss in older adults, including cataracts, age-related macular degeneration, ametropia (presbyopia) and diabetic retinopathy. Patients with senile cataract should be offered a manifest refraction in the early stage, and surgical treatments are indicated when their vision is less than or equal to 0.4. Prevention and treatment of age-related macular degeneration may be achieved through medication or dietary adjustment. Vascular endothelial growth factor can be used in the treatment of neovascularage-related macular degeneration. Patients with presbyopia are advised to obtain a manifest refraction. Patients with diabetic retinopathy should be regularly offered an ocular fundus examination and receive early treatment when necessary, with particular attention paid to glycaemic control. Key words: Vision, binocular; Cataract; Macular degeneration

Diabetic macular edema, retinopathy and age-related macular degeneration as inflammatory conditions.

Diabetic macular edema (DME) and diabetic retinopathy (DR) are complications affecting about 25% of all patients with long-standing type 1 and type 2 diabetes mellitus and are a major cause of significant decrease in vision and quality of life. Age-related macular degeneration (AMD) is not uncommon, and diabetes mellitus affects the incidence and progression of AMD through altering hemodynamics, increasing oxidative stress, accumulating advanced glycation end products, etc. Recent studies suggest that DME, DR and AMD are inflammatory conditions characterized by a breakdown of the blood-retinal barrier, inflammatory processes and an increase in vascular permeability. Key factors that seem to have a dominant role in DME, DR and AMD are angiotensin II, prostaglandins and the vascular endothelial growth factor and a deficiency of anti-inflammatory bioactive lipids. The imbalance between pro- and anti-inflammatory eicosanoids and enhanced production of pro-angiogenic factors may initiate the onset and progression of DME, DR and AMD. This implies that bioactive lipids that possess anti-inflammatory actions and suppress the production of angiogenic factors could be employed in the prevention and management of DME, DR and AMD.

The association between statin use and risk of age-related macular degeneration.

The aim of the present study was to evaluate the association between statin use and the risk of age-related macular degeneration (AMD). A systematic search of the PubMed, EMBASE and ISI web of science databases was used to identify eligible published literatures without language restrictions up to April 2015. Summary relative ratios (RRs) and 95% CIs were estimated using a fixed-effect or random-effects model. A total of 14 studies met the inclusion criteria and were included in this meta-analysis. No significant association was observed between statin use and the risk of any AMD (RR, 0.95; 95% CI, 0.74–1.15); and stratified analysis showed that statins had a significantly different effects on early and late stages of AMD. For early AMD, statin use significantly reduced the risk approximately 17% (RR, 0.83; 95% CI, 0.66–0.99). At the late stage, we observed a significant protective association of statin use with exudative AMD (RR, 0.90; 95% CI, 0.80–0.99), in contrast with the absent association between statins and geographic atrophy (RR, 1.16; 95% CI, 0.77–1.56). These results demonstrated that statin use was protective for early and exudative AMD. Additional large prospective cohort studies and RCTs are required to determine the potential effect of statins on AMD prevention.

Inhibition of Vascular Endothelial Growth Factor Synthesis in Human Retinal Pigment Epithelial Cells by Pazopanib

Age-related macular degeneration (AMD) is a leading cause of central vision blindness in most developed countries. Several new drugs are now available to attempt to prevent progression or treat AMD, however, they have limited effectiveness and therefore are of limited use. Human retinal pigment epithelial (hRPE) cells have been implicated in pathogenesis of AMD via the synthesis of vascular endothelial growth factor (VEGF), which can result in pathological proliferation of vascular endothelial cells and hRPE cells via tyrosine-kinase signaling pathways. Therefore, tyrosine-kinase inhibitors should be considered as potential pharmaco-therapeutic agents in the prevention and treatment of AMD. Since pazopanib (PZB) is a tyrosine-kinase inhibitor of VEGF-R1/VEGF-R2, we investigated its effect on hRPE cell proliferation and VEGF synthesis. We showed that PZB inhibited hRPE cell proliferation and VEGF synthesis in hRPE cells, and therefore it may be of therapeutic value in AMD.

Why lutein is important for the eye and the brain

Lutein and zeaxanthin are carotenoids that accumulate in the macula. The macula is a yellow spot near the center of the retina that is responsible of high resolution vision. Macular pigment acts as a natural blue light filter and protects the eye from damage. Macular pigment optical density (MPOD) increases with lutein administration and is related to visual function and to the prevention of age-related macular degeneration. MOPD can be measured non-invasively and has been related to better cognitive performance. Moreover, compositional analyses of centenarian brains have shown that lutein is the main carotenoid in the brain although not in plasma, indicating a preferential accumulation in neural tissues, and that carotenoids status is correlated with some functional outcomes. Carotenoids are present in human milk with higher concentration in colostrum than in transitional and mature milk. Formula fed-infants have less plasma lutein concentration than breast fed infants. Analyses of brain from infants who died during the first year of life showed that lutein is also the predominant carotenoid of brain. Studies in non-human primates revealed that carotenoids are determinant in the formation of the retinal epithelia. In vitro studies showed that lutein stimulates the differentiation of human stem cells to neural progenitor cells. All this findings together, mostly the presence of lutein in breast milk, plasma concentration in breast-fed infants vs . formula fed infants, preferential accumulation in the brain and evidences of influence on the retina and the functionality of the brain signal the importance of the role of lutein and zeaxanthin on visual maturation and brain development.

Dietary interventions for age‐related macular degeneration: a review of the evidence

PurposeTo summarise the findings of three recently published Cochrane systematic reviews, conducted by the authors that investigated whether taking nutritional supplements can prevent or slow the progression of age‐related macular degeneration (AMD).MethodsThe systematic reviews were performed using standard Cochrane methodology. We included randomised controlled trials (RCTs) where increased dietary intake of omega 3 fatty acids or antioxidant vitamin or mineral supplements were compared to placebo or no intervention with the aim of preventing the development of AMD, or slowing its progression.ResultsThere is no good evidence from RCTs that the general population should be taking antioxidant vitamin supplements to reduce their risk of developing AMD later on in life. By contrast, there is moderate quality evidence that people at high risk of developing advanced AMD may experience a delay in progression by taking specific antioxidant vitamin and mineral supplements. This finding is drawn from trials conducted in the USA in a relatively well‐nourished population. Although observational studies have shown that the consumption of dietary omega 3 fatty acids may reduce the risk of progression to advanced AMD, two recently published RCTs failed to show any benefit of omega 3 supplements on AMD progression.ConclusionsThere is no high quality experimental evidence that nutritional supplementation is beneficial for the primary prevention of AMD. However, people at high risk of developing advanced AMD may benefit from taking antioxidant vitamins. There is currently no evidence to support increasing levels of omega 3 long chain polyunsaturated fatty acids in the diet for the explicit purpose of preventing or slowing the progression of AMD.

Effect of drying, storage temperature and air exposure on astaxanthin stability from Haematococcus pluvialis

Astaxanthin is a powerful antioxidant with various health benefits such as prevention of age-related macular degeneration and improvement of the immune system, liver and heart function. To improve the post-harvesting stability of astaxanthin used in food, feed and nutraceutical industries, the biomass of the high astaxanthin producing alga Haematococcus pluvialis was dried by spray- or freeze-drying and under vacuum or air at −20°C to 37°C for 20weeks. Freeze-drying led to 41% higher astaxanthin recovery compared to commonly-used spray-drying. Low storage temperature (−20°C, 4°C) and vacuum-packing also showed higher astaxanthin stability with as little as 12.3±3.1% degradation during 20weeks of storage. Cost-benefit analysis showed that freeze-drying followed by vacuum-packed storage at −20°C can generate AUD$600 higher profit compared to spray-drying from 100kgH. pluvialis powder. Therefore, freeze-drying can be suggested as a mild and more profitable method for ensuring longer shelf life of astaxanthin from H. pluvialis.

A Decade of Progress in the Understanding, Prevention and Treatment of Age-related Macular Degeneration in Singapore

The year 2014 had marked the 10th anniversary of the nationwide Age-related Macular Degeneration (AMD) Awareness Week in Singapore.1 This public health campaign, organised annually since 2005, aims to generate awareness and understanding of AMD by promoting the importance of education, early detection, and knowledge of treatment and rehabilitation options for the disease. Besides increasing the number of people aged 50 years and older who receive regular eye examinations, the campaign aims to preserve vision and improve the quality of life of individuals affected by AMD and increase the proportion of people with AMD who receive treatment and rehabilitation. At this signifi cant public health milestone, it is timely to review the remarkable decade of progress that has been made in the understanding, prevention and treatment of AMD in Singapore. AMD is the most important cause of irreversible vision loss among people aged 60 years or older in developed countries and accounts for 8.7% of all causes of blindness worldwide.2 It is estimated that by 2020, about 196 million individuals could suffer from AMD globally and this number is likely to rise further to 288 million by 2040.2 The burden of AMD is enormous. Progressive deterioration of central vision from AMD has devastating implications especially when the disease involves both eyes. AMD adversely affects the quality of life with its impact on common vision-related tasks essential for daily living such as reading, recognising faces and driving. Visual loss in the elderly increases the risk of falls, hip fractures and the need for nursing care. It also has negative psychological implications such as depression associated with the visual limitations. The direct costs of managing AMD such as frequent consultations, investigations, repeated treatments and visual rehabilitation is substantial. The indirect costs to society in the form of loss of productivity, unemployment and caregiver expenses make the fi nancial burden of AMD even higher. The fi rst area of major advances in Singapore in the last decade is the considerable improvement in our understanding

Omega 3 fatty acids for preventing or slowing the progression of age-related macular degeneration.

Evidence from animal models and observational studies in humans has suggested that there is an inverse relationship between dietary intake of omega 3 long-chain polyunsaturated fatty acids (LCPUFA) and risk of developing age-related macular degeneration (AMD) or progression to advanced AMD. To review the evidence that increasing the levels of omega 3 LCPUFA in the diet (either by eating more foods rich in omega 3 or by taking nutritional supplements) prevents AMD or slows the progression of AMD. We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (2015, Issue 1), Ovid MEDLINE, Ovid MEDLINE In-Process and Other Non-Indexed Citations, Ovid MEDLINE Daily, Ovid OLDMEDLINE (January 1946 to February 2015), EMBASE (January 1980 to February 2015), Latin American and Caribbean Health Sciences Literature Database (LILACS) (January 1982 to February 2015), the ISRCTN registry (www.isrctn.com/editAdvancedSearch), ClinicalTrials.gov (www.clinicaltrials.gov) and the World Health Organization (WHO) International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). We did not use any date or language restrictions in the electronic searches for trials. We last searched the electronic databases on 2 February 2015. We included randomised controlled trials (RCTs) where increased dietary intake of omega 3 LCPUFA was compared to placebo or no intervention with the aim of preventing the development of AMD, or slowing its progression. Both authors independently selected studies, assessed them for risk of bias and extracted data. One author entered data into RevMan 5 and the other author checked the data entry. We conducted a meta-analysis for one primary outcome, progression of AMD, using a fixed-effect inverse variance model. We included two RCTs in this review, in which 2343 participants with AMD were randomised to receive either omega 3 fatty acid supplements or a placebo. The trials, which had a low risk of bias, were conducted in the USA and France. Overall, there was no evidence that people who took omega 3 fatty acid supplements were at decreased (or increased risk) of progression to advanced AMD (pooled hazard ratio (HR) 0.96, 95% confidence interval (CI) 0.84 to 1.10, high quality evidence). Similarly, people taking these supplements were no more (or less) likely to lose 15 or more letters of visual acuity (USA study HR 0.96, 95% CI 0.84 to 1.10; French study at 36 months risk ratio (RR) 1.25, 95% CI 0.69 to 2.26, participants = 230). The number of adverse events was similar in the intervention and placebo groups (USA study participants with one or more serious adverse event RR 1.00, 95% CI 0.91 to 1.09, participants = 2080; French study total adverse events RR 1.05, 95% CI 0.97 to 1.13, participants = 263). This review found that omega 3 LCPUFA supplementation in people with AMD for periods up to five years does not reduce the risk of progression to advanced AMD or the development of moderate to severe visual loss. No published randomised trials were identified on dietary omega 3 fatty acids for primary prevention of AMD. Currently available evidence does not support increasing dietary intake of omega 3 LCPUFA for the explicit purpose of preventing or slowing the progression of AMD.

Protective Effects of Resveratrol against UVA‐induced Damage in ARPE19 Cells

Exposure to solar ultraviolet (UV) radiation is believed to induce the production of reactive oxygen species (ROS) that may cause oxidative stress to retinal pigment epithelial (RPE) cells; oxidative injury to the retinal pigment epithelium has been implicated to play a contributory role in age‐related macular degeneration (AMD). Prior studies have suggested that resveratrol, an abundant and active component of red grapes, can protect several cell types from oxidative stress. This study is to evaluate if resveratrol can protect RPE cells from UVA induced damage, and be useful in the prevention of early AMD. Cell viability of adult RPE cells pretreated with different concentrations of resveratrol was determined using cell viability assay after UVA radiation. Intracellular H2O2 levels were measured by flow cytometry, and UVA induced signaling pathways were detected using Western blotting. Results show that resveratrol inhibited UVA‐induced RPE cell death. The generation of intracellular H2O2 induced by UVA irradiation in RPE cells was suppressed by resveratrol in a concentration‐dependent manner. In addition, resveratrol inhibited the activation of UVA‐induced extracellular signal‐regulated kinase, c‐jun‐NH2 terminal kinase and p38 kinase in RPE cells. There was also a reduction in UVA‐induced cyclooxygenase‐2 (COX‐2) expression in RPE cells treated with resveratrol. This study suggests that resveratrol is effective in preventing UVA‐induced damage in RPE cells and may be suitable for further developments as a chemoprotective factor for the primary prevention of early AMD.