Lutein is one of the few xanthophyll carotenoids that is found in high concentration in the macula of human retina. As de novo synthesis of lutein within the human body is impossible, lutein can only be obtained from diet. It is a natural substance abundant in egg yolk and dark green leafy vegetables. Many basic and clinical studies have reported lutein’s anti-oxidative and anti-inflammatory properties in the eye, suggesting its beneficial effects on protection and alleviation of ocular diseases such as age-related macular degeneration, diabetic retinopathy, retinopathy of prematurity, myopia, and cataract. Most importantly, lutein is categorized as Generally Regarded as Safe (GRAS), posing minimal side-effects upon long term consumption. In this review, we will discuss the chemical structure and properties of lutein as well as its application and safety as a nutritional supplement. Finally, the effects of lutein consumption on the aforementioned eye diseases will be reviewed.

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The effects of extra virgin olive oil (EVOO) and carbon tetrachloride (CCl) induced oxidative stress in rats were determined by the generation of isoprostanoids. These are known to be robust biomarkers to evaluate nonenzymatic and free radical related oxidation. Other oxidative stress biomarkers such as hydroxyeicosatetraenoic acid products (HETEs) and cholesterol oxidation products (COPs) were also determined. The rodents received a control diet, high-fat diet (20% w/w) composed of extra virgin olive oil (EVOO), corn oil (CO), or lard, and high-fat diets with CCl insult throughout the experimental period. The EVOO diet was found to suppress the formation of isoprostanoids and COPs compared to that of the control. EVOO also had a high total phenolic content and antioxidant activity compared to those of CO and lard and may be contributed to by the hydroxytyrosol component conjugated to fatty acids (HT-FA). This is the first study to identify HT-FA in EVOO, and it was 4-fold higher than that of olive oil, whereas none was found in corn oil. Furthermore, the EVOO diet showed reduced liver lipid vesicles in CCl treated rats compared to that of the control. However, liver toxicity measurements of AST (aspartate transaminase) and ALT (alanine transaminase) activities showed augmentation with CCl treatment but were not alleviated by the diets given. Our findings suggest that EVOO is a daily functional food capable of enhancing the antioxidant system for liver protection; the effect is potentially attributed to the phenolic and lipophenolic (phenol conjugated by fatty acids) content.

Docosahexaenoic acid (DHA), an abundant fatty acid in the brain, is susceptible to auto‐oxidation in situ and releases metabolites such as F4‐neuroprostane (4‐F4t‐NeuroP). The presence of 4‐F4t‐NeuroP in the brain is not well explored. In this study, 4‐F4t‐NeuroP was introduced into neuroblastoma cells (SH‐SY5Y) and, by in vivo infusion, into rodents. Targeted lipidomic analysis of liver and brain tissues shows significant elevation of anti‐inflammatory hydroxylated DHA metabolites and an isomer of neuroprotectin D1, suggesting potential beneficial bioactivities of 4‐F4t‐NeuroP. Additionally, 4‐F4t‐NeuroP treatment in SH‐SY5Y cells and primary neuronal culture consistently upregulates the transcriptional level of the antioxidant enzyme heme oxygenase‐1, but the effect is reduced when 4‐F4t‐NeuroP is further oxidized. Our data suggest that 4‐F4t‐NeuroP could be neuroprotective in the native state but may have disadvantageous bioactivity when oxidized extensively.

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The role of diet and circulatory carotenoids and docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are implicated in age-related macular degeneration (AMD) but not well studied in Chinese. However, other fatty acids were not comprehensively evaluated if it had additional consequence on AMD. This study investigated the relationship among dietary habits, fatty acids levels, carotenoids and AMD in Hong Kong Chinese adults. In this cross-sectional case-controlled study, plasma fatty acids including, saturated fatty acids (SFA), monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), and carotenoids levels were quantified between patients with neovascular AMD (n = 99) and age-gender-matched controls (n = 198). A food frequency questionnaire was also conducted. Low blood carotenoid levels and omega-3 PUFAs namely DHA, EPA and -linolenic acid increased the odds ratio of developing neovascular AMD. High blood omega-6 PUFAs specifically arachidonic acid and eicosadienoic acid, oleic acid (a MUFA) and SFA levels increased the odds ratio of having neovascular AMD. Neovascular AMD group had significantly less omega-3 PUFA rich food (vegetables, nuts, seafood) intake and higher SFA (meat) intake than controls. In short, neovascular AMD was associated with lower circulatory levels of carotenoids and omega-3 PUFAs, and higher level of omega-6 PUFAs, oleic acid and SFAs in the Hong Kong Chinese population. These findings enhance the understandings of dietary impacts on neovascular AMD and provide a context for future nutritional intervention studies.

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