Protective Effects Of Carotenoids Research Articles

Lutein and Zeaxanthin and Their Roles in Age-Related Macular Degeneration-Neurodegenerative Disease.

Lutein and zeaxanthin belong to the xanthophyll family of carotenoids, which are pigments produced by plants. Structurally, they are very similar, differing only slightly in the arrangement of atoms. Key sources of these carotenoids include kale, savoy cabbage, spinach, broccoli, peas, parsley, corn, and egg yolks. The recommended daily intake of lutein is approximately 10.0 mg and that of zeaxanthin is 2 mg. Lutein intake in adults varies, with average intakes being 1–2 mg/day. Due to the lack of synthesis of consumption of these compounds in humans, these substances are extremely important for the proper functioning of certain organs of the body (eye, skin, heart, intestines). Eating a lot of dark leafy vegetables and some fruits can help to prevent our bodies from developing diseases. The protective effects of carotenoids are mainly related to their defense against oxidative stress and their ability to scavenge free radicals. Lutein and zeaxanthin are the only dietary carotenoids that accumulate in the retina, specifically the macula, and are called macular pigments. These carotenoids are concentrated by the action of specific binding proteins such as StARD3, which binds lutein, and GSTP1, which binds zeaxanthin and its dietary metabolite, mesozeaxanthin. It has been shown that supportive therapy with lutein and zeaxanthin can have a beneficial effect in delaying the progression of eye diseases such as age-related macular degeneration (AMD) and cataracts. This article presents the current state of knowledge on the role of lutein and zeaxanthin, especially from human studies targeting their metabolism and bioavailability, with recommendations to consume xanthophyll-rich foods.

The Associations of Plasma/Serum Carotenoids with Alzheimer's Disease: A Systematic Review and Meta-Analysis.

Multiple lines of evidence indicate protective effects of carotenoids in Alzheimer's disease (AD). However, previous epidemiological studies reported inconsistent results regarding the associations between carotenoids levels and the risk of AD. Our study aims to evaluate the associations of six major members of carotenoids with the occurrence of AD by conducting a systematic review and meta-analysis. Following PRISMA guidelines, a comprehensive literature search of PubMed, Web of Science, Ebsco, and PsycINFO databases was conducted, and the quality of each included studies was evaluated by a validated scoring systems. Standardized mean differences (SMD) with 95% confidence intervals (CI) were determined by using a random effects model. Heterogeneity was evaluated by I2 statistics. Publication bias was detected using funnel plots and Egger's test. Sixteen studies, with 10,633 participants were included. Pooled analysis showed significantly lower plasma/serum levels of lutein (SMD = -0.86, 95% CI: -1.67 to -0.05, p = 0.04) and zeaxanthin (SMD = -0.59; 95% CI: -1.12 to -0.06, p = 0.03) in patients with AD versus cognitively intact controls, while α-carotene (SMD = 0.21, 95% CI: -0.68 to 0.26, p = 0.39), β-carotene (SMD = 0.04, 95% CI: -0.57 to 0.65, p = 0.9), lycopene (SMD = -0.12, 95% CI: -0.96 to 0.72, p = 0.78), and β-cryptoxanthin (SMD = -0.09, 95% CI: -0.83 to 0.65, p = 0.81) did not achieve significant differences. Of six major members of carotenoids, only lutein and zeaxanthin concentrations in plasma/serum were inversely related to the risk of AD. More high-quality longitudinal studies are needed to verify these findings.

Protective effects of carotenoids and retinoids on benzo[a]pyrene induced mutagenicity and oxidative stress

Protective effects of carotenoids and retinoids on benzo[a]pyrene induced mutagenicity and oxidative stress

Serum carotenoids in relation to risk factors for development of atherosclerosis

ObjectiveTo explore associations between serum carotenoids and risk factors for development of atherosclerosis. Design and methodsWe studied 40 early atherosclerosis patients without clinical cardiovascular events and comparable healthy controls aged 45–68years. Intima-media thickness (IMT) and arterial stiffness were simultaneously measured by carotid ultrasonography, and serum carotenoids and cytokines were determined by high-pressure liquid chromatograph (HPLC) and ELISA kits respectively. We evaluated the associations between serum carotenoids, early atherosclerosis and serum cytokines. ResultsSerum concentrations of lutein and zeaxanthin in early atherosclerosis patients were significantly lower than those of control subjects. PCA logistic analysis found that serum carotenoids were associated with decreased risk of atherosclerosis. In contrast, blood pressure, body mass index and serum triglyceride were positively related to the risk of atherosclerosis. Ridge regression analysis revealed that serum carotenoids were associated with inflammatory cytokines and apoE. More specifically, serum lutein was inversely associated with IL-6 (P<0.001) and positively associated IFN-γ (P=0.002). In contrast, zeaxanthin had a significant negative association with VCAM-1 (P=0.001) and apoE (P=0.022) .Lycopene was inversely associated with VCAM-1(P=0.011) and LDL (P=0.046). ConclusionsThe results suggested that early atherosclerosis patients had lower serum concentrations of lutein and zeaxanthin than healthy subjects. Serum carotenoids were associated with reduced risk of atherosclerosis. The associations between serum carotenoids and inflammatory cytokines may help to explain the possible protective effects of carotenoids on atherosclerosis.

Animal Models in Carotenoids Research and Lung Cancer Prevention

Numerous epidemiological studies have consistently demonstrated that individuals who eat more fruits and vegetables (which are rich in carotenoids) and who have higher serum β-carotene levels have a lower risk of cancer, especially lung cancer. However, two human intervention trials conducted in Finland and in the United States have reported contrasting results with high doses of β-carotene supplementation increasing the risk of lung cancer among smokers. The failure of these trials to demonstrate actual efficacy has resulted in the initiation of animal studies to reproduce the findings of these two studies and to elucidate the mechanisms responsible for the harmful or protective effects of carotenoids in lung carcinogenesis. Although these studies have been limited by a lack of animal models that appropriately represent human lung cancer induced by cigarette smoke, ferrets and A/J mice are currently the most widely used models for these types of studies. There are several proposed mechanisms for the protective effects of carotenoids on cigarette smoke-induced lung carcinogenesis, and these include antioxidant/prooxidant effects, modulation of retinoic acid signaling pathway and metabolism, induction of cytochrome P450, and molecular signaling involved in cell proliferation and/or apoptosis. The technical challenges associated with animal models include strain-specific and diet-specific effects, differences in the absorption and distribution of carotenoids, and differences in the interactions of carotenoids with other antioxidants. Despite the problems associated with extrapolating from animal models to humans, the understanding and development of various animal models may provide useful information regarding the protective effects of carotenoids against lung carcinogenesis.

Carotenoid Supplementation Reduces Erythema in Human Skin After Simulated Solar Radiation Exposure

Abstract. Excessive exposure to solar radiation, especially ultraviolet A (UVA: 320–400 nm) and ultraviolet B (UVB: 290–320 nm) radiation, may induce UV-carcinogenesis and erythema in the skin. Although the protective effects of carotenoids against skin lesions are still unclear, β-carotene has been proposed as an oral sun protectant. The purpose of this study was to determine the magnitude of the protective effects of oral α- and β-carotene supplementation for 24 weeks on UVA- and UVB-induced erythema in humans. While being exposed to UVA and UVB radiation, 22 subjects (11 men and 11 women) were supplemented with natural carotenoids for 24 weeks. Each day for the first 8 weeks, subjects were given 30 mg of natural carotenoids containing 29.4 mg of β-carotene, 0.36 mg of α-carotene, and traces of other carotenoids in vegetable oil. The natural carotenoid dose was progressively raised by 30-mg increments, at every 8 weeks, from 30 mg to 90 mg. Small areas (1 cm2) of the skin were exposed to increasing doses of UV light (16–42 mJ/cm2) to determine the minimal erythema dose (MED). MED was defined as a uniform pink color with well-defined borders. MED readings were obtained by visual inspection 24 hr postirradiation. Blood samples taken during supplementation were used to determine α- and β-carotene serum levels and for a lipid peroxidation analysis. During natural carotenoid supplementation, the MED of solar simulator radiation increased significantly (P < 0.05). After 24 weeks of supplementation, serum β-carotene levels were increased from 0.22 μg/ml (95% CI; 0.16–0.27) to 1.72 μg/ml (95% CI;1.61–1.83). Similarly, α-carotene serum levels increased from 0.07 μg/ml (95% CI;0.048–0.092) to 0.36 μg/ml (95% CI; 0.32–0.40). Serum lipid peroxidation was significantly (P < 0.05) inhibited in a dose-dependent manner during natural carotenoid supplementation. The present data suggest that supplementation with natural carotenoids may partially protect human skin from UVA- and UVB-induced erythema, although the magnitude of the protective effect is modest.

Protective effects of carotenoids from saffron on neuronal injury in vitro and in vivo

Crocus sativus L. (saffron) has been used as a spice for flavoring and coloring food preparations, and in Chinese traditional medicine as an anodyne or tranquilizer. Our previous study demonstrated that crocin, a carotenoid pigment of saffron, can suppress the serum deprivation-induced death of PC12 cells by increasing glutathione (GSH) synthesis and thus inhibiting neutral sphingomyelinase (nSMase) activity and ceramide formation. The carotenoid pigments of saffron consist of crocetin di-(β- d-glucosyl)-ester [dicrocin], crocetin-(β- d-gentiobiosyl)-(β- d-glucosyl)-ester [tricrocin] and crocetin-di-(β- d-gentiobiosyl)-ester [crocin]. Saffron also contains picrocrocin, the substance causing saffron's bitter taste. In this study, to confirm whether neuroprotective effects of saffron are caused solely by crocin, we examined the antioxidant and GSH-synthetic activities of these crocins in PC12 cells under serum-free and hypoxic conditions. Measurements of cell viability, peroxidized membrane lipids and caspase-3 activity showed that the rank order of the neuroprotective potency at a concentration of 10 μM was crocin > tricrocin > dicrocin and picrocrocin (the latter two crocins had a little or no potency). In addition, we show that among these saffron's constituents, crocin most effectively promotes mRNA expression of γ-glutamylcysteinyl synthase (γ-GCS), which contributes to GSH synthesis as the rate-limiting enzyme, and that the carotenoid can significantly reduce infarcted areas caused by occlusion of the middle cerebral artery (MCA) in mice.

Carotenoids and Protection against Solar UV Radiation

Upon exposure to UV light photooxidative reactions are initiated which are damaging to biomolecules and affect the integrity of cells and tissues. Photooxidative damage plays a role in pathological processes and is involved in the development of disorders affecting the skin. When skin is exposed to UV light, erythema is observed as an initial reaction. Carotenoids like β-carotene or lycopene are efficient antioxidants scavenging singlet molecular oxygen and peroxyl radicals generated in during photooxidation. When β-carotene was applied as such or in combination with α-tocopherol for 12 weeks, erythema formation induced with a solar light simulator was diminished from week 8 on. Similar effects were also achieved with a diet rich in lycopene. Ingestion of tomato paste corresponding to a dose of 16 mg lycopene/ day over 10 weeks led to increases in serum levels of lycopene and total carotenoids in skin. At week 10, erythema formation was significantly lower in the group that ingested the tomato paste as compared to the control group. No significant difference was found at week 4 of treatment. Thus, protection against UV light-induced erythema can be achieved by ingestion of a commonly consumed dietary source of lycopene. Such protective effects of carotenoids were also demonstrated in cell culture. The in-vitro data indicate that there is an optimal level of protection for each carotenoid.

44] Carotenoids in human skin: Noninvasive measurement and identification of dermal carotenoids and carotenol esters

Skin is the major light-exposed tissue and thus is susceptible to photooxidative stress. In vitro studies demonstrated that carotenoids interact with light of different wavelengths and are capable of scavenging reactive oxygen species, especially those formed in photooxidative reactions. Carotenoids efficiently scavenge singlet molecular oxygen and excited triplet carbonyls, which are formed on photoexcitation of sensitizer molecules. Protective effects of carotenoids in the skin were shown in the treatment of a genetic disorder, erythropoietic protoporphyria. In this disease, exceptionally high amounts of the photosensitizer protoporphyrin generate reactive intermediates in photooxidative reactions. The excited sensitizers and/or subsequently formed reactive triplet carbon species or singlet molecular oxygen are the reactive agents responsible for damaging reactions with biological macromolecules. The symptoms of erythropoietic protoporphyria are alleviated on treatment with high doses of β-carotene. Dermal accumulation of β-carotene attracted attention, as it has been speculated that carotenoids contribute to protection against acute and chronic exposure to ultraviolet (UV) light. Although the protective effects of carotenoids toward skin lesions are still under investigation, β-carotene supplements are in use as oral sun protectants. Little is known about the accumulation of carotenoids in skin and their distribution in various skin areas. The dermal levels of carotenoids can be measured noninvasively by reflection photometry, which was used to follow β-carotene levels in skin after supplementation.