Dose Of Lutein Research Articles

Lutein Emulsion Stabilized by a Food-Grade Biopolymer Enhanced Lutein Bioavailability and Improved Retinal Vessel Morphology in Neonatal Rats with Retinopathy of Prematurity

BackgroundRetinopathy of prematurity (ROP) is a leading cause of blindness in infants, affecting 32% of hospitalized preterm babies. Oxidative stress, a primary pathogenic factor in ROP, triggers abnormal neovascularization of retinal vessels. Lutein, an antioxidant and the main component of macular pigment, is found in low levels in preterm infants and may help ameliorate ROP. However, its low bioavailability limits its application as a nutritional intervention. ObjectiveThe aim of the study was to assess the effect of a lutein emulsion stabilized by a food-grade biopolymer on lutein bioavailability in neonatal rats with ROP and examine the effects of both unemulsified lutein and lutein emulsion on the disease. MethodsNeonatal rats were subcutaneously administered KRN 633 (10 mg/kg BW) on postnatal days 7 and 8 (P7 and P8) to induce ROP. Neonatal rats that did not receive the treatment served as the control. From P9 to P21, both ROP and non-ROP rats were divided into three groups and given daily doses of olive oil, unemulsified lutein (2 mg/kg BW lutein), or lutein emulsion (2 mg/kg BW lutein). On P22, serum and tissues were collected. Lutein concentrations were measured using UPLC, and retinal morphology was assessed using immunohistochemistry. ResultsRats treated with lutein emulsion had significantly higher serum and tissue lutein concentrations than those receiving unemulsified lutein. Morphological assessments showed that ROP rats had more tortuous arteries, increased capillary density, enlarged vessels, reduced astrocyte density, and decreased neuronal cells. Both unemulsified lutein and lutein emulsion alleviated these abnormalities, with lutein emulsion showing superior efficacy in restoring neuronal cell levels to normal in the peripheral retina. ConclusionsLutein, in both unemulsified and emulsified forms, effectively inhibited ROP progression in neonatal rats. The biopolymer-based lutein emulsion showed promise as a delivery system to enhance lutein bioavailability and mitigate ROP in preterm infants.

Histological and Biochemical Effects of Lutein on Paraquat-induced Renal Toxicity in Wistar Rats

Introduction: Paraquat (PQ) poisoning in humans predominantly results from the generation of reactive oxygen species (ROS). To date, no proven antidote exists for PQ poisoning, which is characterized by severe kidney injury and high mortality rates globally. However, free radical scavengers and antioxidant agents have shown potentials to mitigate PQ toxicity. Aim: The study is aimed at investigating lutein, an antioxidant, for possible mitigation of paraquat-induced renal toxicity. Study Design: Preclinical experimental study. Place and Duration of Study: Department of Anatomy, Obafemi Awolowo University (OAU), Nigeria, between 2022 and 2023. Methods: Forty wistar rats weighing 150-180 grammes were randomly grouped (A to E) for this study. Paraquat (PQ) toxicity was induced in groups B to E. Lutein was administered at graded doses of 50 mg/kg, 100 mg/kg and 150 mg/kg to groups C to E for twenty-one days respectively. Group A (positive control) was given only normal saline, while group B had paraquat only. Twenty-four hours after the last administration, urine and blood samples were collected and the animals were sacrificed before the excision of the kidneys. Results: A marked histological distortion, which was characterized by compromised Bowman's space and renal tubule dimensions, was observed in Group B. In contrast, the lutein-treated groups exhibited dose-dependent improvements, with outcomes comparable to the control group. Notably, Group B showed significant elevations in plasma creatinine (P = 0.003) and urine protein (P = 0.001), accompanied by reduced plasma protein (P = 0.004), relative to the treated groups. However, Group E, which received the highest lutein dose, demonstrated substantial improvement in histoarchitectural and biochemical findings similar to the control group." Conclusion: This study demonstrated significant alterations in the histoarchitecture and biochemical profiles of renal tissue following paraquat exposure. Notably, the lutein-treated groups exhibited substantial improvement, with results comparable to the control group. These findings suggest that lutein may possess potential therapeutic properties to mitigate paraquat-induced renal toxicity.

Effects of Lutein on the Body Weights, Hepato-renal DNA and Antioxidant Capacity Following Paraquat-induced Toxicity in Wistar Rats

Introduction: Paraquat is a leading cause of herbicide-related fatalities worldwide. Its high mortality rate is attributed to its inherent generation of ROS-mediated toxicity, and lack of effective treatment till date. Lutein is an antioxidant with free radical scavenging ability, which may contribute to its protective effects and possible DNA preservation. Objective: The study is evaluating the effects of lutein on body weights and hepato-renal antioxidant capacity with DNA quantification following paraquat toxicity in wistar rats. Methods: Thirty-five male Wistar rats (150-180g) rats were randomly divided into five equal groups (A-E). Paraquat toxicity was induced in Groups B-E with 5mg/kg for three days. Group A received normal saline only, while Group B was given paraquat only. Thereafter, Groups C-E received varying doses of lutein (50, 100, 150mg/kg) for 21 days. Their body weights were recorded twice weekly using a digital balance. The animals were sacrificed and their liver with kidneys were excised and processed. The photomicrographs were taken at various magnifications while Image J software was employed for DNA densities. The total antioxidant capacity (TAC) was assessed by Prieto method. Results: There was significant reductions in the body weights, (p=0.00) hepato-renal DNA densities (p=0.00, p=0.01) and antioxidant capacities of the PQ-only group relative to the positive control A in both liver and kidneys (p-0.01, p=0.02). However, the lutein-treated groups had dose-dependent similar features with the control, which had normal histo-morphological feature. The highest dose of lutein showed the best correlation with the control. Conclusion: This study showed significant alterations in body weights, hepato-renal DNA densities and antioxidant capacities especially in the PQ-only group. Meanwhile, the lutein-treated groups, especially at high dosages, showed significant improvements in the indices similar to the control. Hence, lutein may be a useful agent for attenuating paraquat toxicity.

Utilization of Biopolymer-Based Lutein Emulsion as an Effective Delivery System to Improve Lutein Bioavailability in Neonatal Rats.

Newborns' eyes and brains are prone to oxidative stress. Lutein has antioxidant properties and is the main component of macular pigment essential for protecting the retina, but has low bioavailability, thereby limiting its potential as a nutritional supplement. Oil-in-water emulsions have been used as lutein delivery systems. In particular, octenylsuccinated (OS) starch is a biopolymer-derived emulsifier safe to use in infant foods, while exhibiting superior emulsifying capacity. This study determined the effects of an OS starch-stabilized lutein emulsion on lutein bioavailability in Sprague-Dawley neonatal rats. In an acute study, 10-day-old pups received a single oral dose of free lutein or lutein emulsion, with subsequent blood sampling over 24 h to analyze pharmacokinetics. The lutein emulsion group had a 2.12- and 1.91-fold higher maximum serum lutein concentration and area under the curve, respectively, compared to the free lutein group. In two daily dosing studies, oral lutein was given from postnatal day 5 to 18. Blood and tissue lutein concentrations were measured. The results indicated that the daily intake of lutein emulsion led to a higher lutein concentration in circulation and key tissues compared to free lutein. The OS starch-stabilized emulsion could be an effective and safe lutein delivery system for newborns.

Lutein Can Alleviate Oxidative Stress, Inflammation, and Apoptosis Induced by Excessive Alcohol to Ameliorate Reproductive Damage in Male Rats.

Chronic excessive alcohol intake may lead to male reproductive damage. Lutein is a carotenoid compound with antioxidant activity. The purpose of this study was to observe the effect of lutein supplementation on male reproductive damage caused by excessive alcohol intake. In this study, an animal model of excessive drinking (12 mL/(kg.bw.d)) for 12 weeks was established and supplemented with different doses of lutein (12, 24, 48 mg/(kg.bw.d)). The results showed that the body weight, sperm quality, sex hormones (FSH, testosterone), and antioxidant markers (GSH-Px) decreased significantly, while MDA and inflammatory factors (IL-6, TNF-α) increased significantly in the alcohol model group when compared to the normal control group. After 12 weeks of high-dose lutein supplementation with 48mg/(kg.bw.d), the spermatogenic ability, testosterone level, and the activity of marker enzymes reflecting testicular injury were improved. In addition, high-dose lutein supplementation downregulated the NF-κB and the pro-apoptosis biomarkers (Bax, Cytc and caspase-3), whereas it upregulated the expression of Nrf2/HO-1 and the anti-apoptotic molecule Bcl-2. These findings were fully supported by analyzing the testicular histopathology and by measuring germ cell apoptosis. In conclusion, lutein protects against reproductive injury induced by excessive alcohol through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Functional Characterization of Marigold Powder as a Food Ingredient for Lutein-Fortified Fresh Noodles

Marigold powder was utilized as a food ingredient to produce lutein-fortified fresh noodles for eye health, and its functionalities were characterized in terms of thermo-rheological, structural, and antioxidant properties. The pasting parameters and starch-gelatinization enthalpy values of wheat flour had a tendency to decrease with increasing levels of marigold powder. The use of marigold powder led to decreases in the storage and loss moduli of wheat flour pastes by weakening their cellular microstructure, which was confirmed by the scanning electron microscopic images. When marigold powder was incorporated into the formulation of fresh noodles, the cooking loss and water absorption of the noodles were not negatively affected at a level of 2% (w/w). Also, the noodles with 2% marigold powder were not significantly different from the control for the maximum resistance to extension. The levels of lutein in the noodles prepared with marigold powder (61.2 to 204.9 mg/100 g) were reduced by almost 50% after cooking. However, they seemed to satisfy the recommended daily dose of lutein for visual functions. Moreover, the use of marigold powder provided antioxidant properties for noodles by enhancing the 2,2′-diphenyl-1-picrylhydrazyl (DPPH) and 2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) radical-scavenging activities.

Possible Protective Effects of high- versus low- dose of lutein in combination with irinotecan on Liver of Rats: Role of Oxidative Stress and Apoptosis

Objectives: The current study was designed to describe roles of oxidative stress via the measurementof malondialdehyde and total antioxidant markers, and apoptosis through the measurement of caspase 3marker, as mechanisms of liver toxicity induced by irinotecan; and to explore the possible protective effectsof high- and low- doses of lutein against irinotecan induced toxicity in the liver of rats.Methods: Thirty six (36) Sprague-Dawley rats were randomly divided into six groups: Groups ?, ratsreceived single oral daily dose of dimethyl sulfoxide (4 ml/kg); Group ?? (irinotecan-treated), receivedsingle oral daily dose of dimethyl sulfoxide (4ml/kg) for 25 days by oral gavage and subsequently receivedirinotecan (50mg/kg) on days: 5, 10, 15 (total dose=150 mg/kg) by intraperitoneal injection; Groups ???and ?V, received oral dose of lutein (6mg/kg/day) and (24mg/kg/day), respectively by oral gavage for 25successive days (lutein-treated); Groups V and V? (lutein+ irinotecan), received oral dose of lutein (6mg/kg/day) and (24mg /kg/day), respectively by oral gavage for 25 successive days, and subsequently receivedirinotecan (50mg /kg body weight) on days: 5, 10, 15 (total dose=150 mg/kg) by intraperitoneal injection.Results: Orally-administered lutein with total cumulative dose of irinotecan (Groups V and VI), resultedin significant reduction (P<0.05) of serum aspartate aminotransferase and alanine aminotransferase, andsignificant reduction (P<0.05) of malondialdehyde; but, significant elevation (P<0.05) of serum totalantioxidant capacity; and there was significant reduction in caspase 3in liver tissues homogenates comparedto the corresponding levels in the group of rats administered irinotecan (Group II).Conclusion: Results of the current finding suggested that administration of lutein may be a useful compoundthat alleviated irinotecan induced toxicity to the liver

Protective effect of lutein on oxidative stress damage caused by acute PM2.5 exposure in rats

Particulate matter (PM) is the sum of organic and inorganic substances suspended in air. Particles with a diameter equal to or smaller than 2.5 μm (PM2.5) can induce extensive oxidative stress damage in lung tissues. Lutein can prevent oxidative stress and the production of pro-inflammatory cytokines. However, its role in lung injury induced by PM2.5 is still unclear. This study used lutein to intervene in lung injury induced by PM2.5 in rats to confirm the protective function of lutein in PM2.5- induced lung injury. A total of 80 rats were divided into five groups according to body weight (bw). Rats in the blank control group and the PM2.5 exposure group were treated with normal saline. The low-, medium-, and high-dose lutein groups were treated with 12.5, 25.0, and 50.0 mg/kg·bw lutein continuously for 28 days. In addition, on days 22-28, 10 mg/kg PM2.5 was introduced by intratracheal instillation into the PM2.5 exposure group and all lutein dose groups continuously for 7 days to establish PM2.5 injury models. Lung tissues were collected and subjected to hematoxylin-eosin (HE) staining to observe histomorphological changes. Bronchoalveolar lavage fluid (BALF) was collected to detect the expression of cell damage indicators including lactate dehydrogenase (LDH), acidic phosphatase (ACP), alkaline phosphatase (AKP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α). In addition, the levels of serum oxidative stress indicators in rats, including methane dicarboxylic aldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide synthase (NOS), and 8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as cytokines, including IL-6, IL-8, and TNF-α, were analyzed. Lung tissues of rats after PM2.5 exposure exhibited different degrees of pathological changes. In serum, oxidative damage indicators MDA, NOS, and 8-OHdG and inflammatory cytokines IL-6, IL-8, and TNF-α significantly increased whereas GSH levels significantly decreased (P<0.05). In BALF, cell damage indicators ACP and AKP and inflammatory cytokines IL-6, IL-8, and TNF-α all increased (P<0.05). After lutein intervention, oxidative damage and cellular inflammatory cytokines in serum and BALF all significantly decreased (P<0.05) whereas serum GSH levels increased (P<0.05). PM2.5 caused significant oxidative damage and inflammatory injury in rat lungs. Lutein alleviated these effects, playing a protective role in lung tissues.

Effect Of Lutein from Chlorella pyrenoidosa INK On The Activities And Phagocytic Capacity On Peritoneal Macrophage Cells Of Mice Infected With Staphylococcus aureus

Chlorella pyrenoidosa is a microalgae that produce lutein compounds that can stimulate an immune response. This study examined the crude lutein extracted from biomass C. pyrenoidosa INK as an immunomodulator through observation activity and phagocytic capacity of peritoneal macrophages of mice. This study uses twenty-eight mice were divided into 7 groups each comprising 4 replicates ie Group (I) normal controls, mice were untreated(II) a negative control, mice were induced by Staphylococcus aureus; (III) positive control, mice were induced by S. aureus and treatment of meniran extract (Phyllanthus niruri, stimuno®). The treatment group (IV-VII), mice were induced by S. aureus and treatment of crude lutein, respectively: 0.058 mg, 0.117 mg, 0.234 mg and 0.468 mg per 20 g of body weight. Lutein crude was given for 2 weeks and the next day the mice were injected bacterium S aureus. The results showed that crude lutein from C. pyrenoidosa INK act as immunomodulators that can stimulate an immune response as the dose increases. Treatment of crude lutein dose of 0.234 mg per 20 g BW of mice showed a proportional response to the positive control treatment (stimuno®). Lutein of C.pyrenoidosa had a positive effect on the the activity and capacity of peritoneal macrophage in mice after stimulation with S. aureus bacteria.

Effect of carotenoid class and dose on the larval growth and development of the critically endangered southern corroboree frog.

Dietary carotenoids are expected to improve vertebrate growth and development, though evidence for beneficial effects remains limited. One reason for this might be that few studies have directly compared the effects of carotenoids from different classes (carotenes versus xanthophylls) at more than one dose. Here, we tested the effect of two doses of dietary β-carotene and lutein (representing two different carotenoid classes) on the growth and development of larval southern corroboree frogs (Pseudophryne corroboree). Individuals were supplemented with either β-carotene or lutein at one of two doses (0.1 mg g-1, 1 mg g-1), or given a diet without carotenoids (control). Each dietary treatment included 36 replicate individuals, and individuals remained on the same diet until metamorphosis (25-39 weeks). We measured larval survival, larval growth (body length), time to metamorphosis, metamorphic body size (mass and SVL), and body condition. Lutein had no detectable effect on larval growth and development. However, larvae receiving a high dose (1 mg g-1) of β-carotene metamorphosed significantly faster than all other dietary treatments, despite no significant differences in growth rate. This result indicates that β-carotene supplementation in P. corroboree has positive effects on development independent of growth effects. Our study provides new evidence for differential effects of carotenoid class and dose on vertebrate development. From a conservation perspective, our findings are expected to assist with the recovery of P. corroboree by expediting the generation of frogs required for the maintenance of captive insurance colonies, or the provision of frogs for release. More broadly, our study highlights the potential for dietary manipulation to assist with the ex situ management of threatened amphibian species worldwide.

13C-lutein is differentially distributed in tissues of an adult female rhesus macaque following a single oral administration: a pilot study

Despite the growing awareness regarding lutein's putative roles in eyes and brain, its pharmacokinetics and tissue distribution in primates have been poorly understood. We hypothesized that 13C-lutein will be differentially distributed into tissues of an adult rhesus macaque (Macaca mulatta) 3 days following a single oral dose. After a year of prefeeding a diet supplemented with unlabeled lutein (1 μmol/kg/d), a 19-year-old female was dosed with 1.92 mg of highly enriched 13C-lutein. Tissues of a nondosed, lutein-fed monkey were used as a reference for natural abundance of 13C-lutein. On the third day postdose, plasma and multiple tissues were collected. Lutein was quantified by high-performance liquid chromatography–photodiode array detector, and 13C-lutein tissue enrichment was determined by liquid chromatography quadrupole time-of-flight mass spectrometry. In the tissues of a reference monkey, 12C-lutein with natural abundance of 13C-lutein was detectable. In the dosed monkey, highly enriched 13C-lutein was observed in all analyzed tissues except for the macular and peripheral retina, with the highest concentrations in the liver followed by the adrenal gland and plasma. 13C-lutein accumulated differentially across 6 brain regions. In adipose depots, 13C-lutein was observed, with the highest concentrations in the axillary brown adipose tissues. In summary, we evaluated 13C-lutein tissue distribution in a nonhuman primate following a single dose of isotopically labeled lutein. These results show that tissue distribution 3 days following a dose of lutein varied substantially dependent on tissue type.

Mono- and diglycerides improve lutein absorption in healthy adults: a randomised, double-blind, cross-over, single-dose study.

With the association between increased carotenoid intake and lower risk of chronic diseases, the absorption of lutein from the diet becomes an important factor in its delivery and physiological action. The primary objective of this study was to gain an understanding of how a new formulation technology (mixture of mono- and diglycerides (MDG)), affected lutein absorption. Subjects (n 24) were randomised in a cross-over, double-blind study to receive a single dose of 6 mg lutein (FloraGLO 20 %) provided as capsules containing either high-oleic safflower (SAF) oil or a MDG oil. Subjects receiving a single dose of lutein in MDG showed a significantly greater change from baseline (0 h) to 4, 6, 8, 12, 24, 48 and 336 h (P<0·05) and baseline adjusted AUC for plasma lutein at 48 and 336 h (P<0·001) as compared with subjects given lutein in SAF. Analysis of the 48 h absorption kinetics of lutein showed that the time to peak level of lutein (12 h) was the same for SAF and MDG groups, but the change in plasma lutein at 12 and 48 h were 129 and 320 % higher, respectively, for MDG compared with SAF. This difference continued as the adjusted AUC 0-48 and 0-336 h for the MDG group was 232 and 900 % higher, respectively, v. SAF. The study data show that by changing the lipid that is combined with a lutein supplement results in significant increases in lutein absorption in healthy adults.

Lutein improves cell viability and reduces Alu RNA accumulation in hydrogen peroxide challenged retinal pigment epithelial cells

Purpose: Dysfunction of the microRNA (miRNA)-processing enzyme DICER1 and Alu RNA accumulation are linked to the pathogenesis of age-related macular degeneration (AMD). This study determined the optimal dose of lutein (LUT) and zeaxanthin (ZEA) to protect human retinal pigment epithelium (RPE) cells against hydrogen peroxide (H2O2). The effect of the optimal dose of LUT and ZEA as DICER1 and Alu RNA modulators in cultured human RPE cells challenged with H2O2 was investigated.Materials and methods: ARPE-19 cells were pre-treated with LUT, ZEA, or both for 24 h before 200 μM H2O2 challenge. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. DICER1 and Alu RNA were quantified by western blotting and real-time polymerase chain reaction, respectively.Results: H2O2 increased cell Alu RNA expression and decreased cell viability of ARPE-19, but had no significant impact on the DICER1 protein level. LUT, alone and in combination with ZEA pre-treatment, prior to H2O2 challenge significantly improved cell viability of ARPE-19 and reduced the level of Alu RNA compared to the negative control.Conclusions: These results support the use of LUT alone, and in combination with ZEA, in AMD prevention and treatment. This study is also the first to report LUT modulating effects on Alu RNA.

Nanoencapsulation of lutein and its effect on mice's declarative memory

Lutein is a xanthophyll carotenoid widely known by its biological properties and low toxicity. When located in the brain, lutein may inhibit damage mechanisms, acting in neural cells maintenance. However, this carotenoid is very sensitive to external agents such as heat, light, pH and oxidation, besides presenting low absorption in gastrointestinal tract due its low solubility in water. Encapsulation procedures have shown promising results to increase lutein stability and bioavailability. In this work, lutein was encapsulated in polyvinylpyrrolidone (PVP) matrix by the dissolution in common solvent method. Nanoparticles were characterized in respect to morphology, water solubility, and interactions between PVP and lutein. In vivo tests were carried out in order to investigate the influence of lutein encapsulation on mice's declarative memory. Ex vivo tests were also carried out to determine if nanoparticles may cause any inflammatory process per se. Results indicated that lutein was successfully encapsulated in PVP while nanoparticles presented spherical shape and uniform size. Encapsulation was able to increase water solubility of lutein by more than 43 times, which may be attributed to the formation of soluble complexes trough hydrogen bonds between lutein hydroxyl group and PVP carbonyl group. In vivo studies showed that the administration of free lutein at 100mg·kg−1 and lutein-loaded PVP nanoparticles at 10 and 1.5mg·kg−1 significantly increased mice's object recognition index, meaning that significant lower doses of lutein were needed to achieve the same effect when lutein was encapsulated. Ex vivo studies showed that lutein-loaded nanoparticles administration did not alter inflammatory parameters in plasma, liver and brain of mice. In this sense, lutein-loaded PVP nanocapsules showed to be an advantageous alternative to increase water solubility and to improve the memory of mice without causing inflammatory damage per se.

Carrot solution culture bioproduction of uniformly labeled 13C-lutein and invivo dosing in non-human primates.

Lutein is a xanthophyll abundant in nature and most commonly present in the human diet through consumption of leafy green vegetables. With zeaxanthin and meso-zeaxanthin, lutein is a component of the macular pigment of the retina, where it protects against photooxidation and age-related macular degeneration. Recent studies have suggested that lutein may positively impact cognition throughout the lifespan, but outside of the retina, the deposition, metabolism, and function(s) of lutein are poorly understood. Using a novel botanical cell culture system ( Daucus carota), the present study aimed to produce a stable isotope lutein tracer for use in future investigations of dietary lutein distribution and metabolism. Carrot cultivars were initiated into liquid solution culture, lutein production conditions optimized, and uniformly labeled 13C-glucose was provided as the sole media carbon source for four serial growth cycles. Lutein yield was 2.58 ± 0.24 µg/g, and mass spectrometry confirmed high enrichment of 13C: 64.9% of lutein was uniformly labeled and 100% of lutein was labeled on at least 37 of 40 possible carbons. Purification of carrot extracts yielded a lutein dose of 1.92 mg with 96.0 ± 0.60% purity. 13C-lutein signals were detectable in hepatic extracts of an adult rhesus macaque monkey ( Macaca mulatta) dosed with 13C-lutein, but not in hepatic samples collected from control animals. This novel botanical biofactory approach can be used to produce sufficient quantities of highly enriched and pure 13C-lutein doses for use in tracer studies investigating lutein distribution, metabolism, and function.

Molecular mechanism of lutein protecting Müller cells against oxidative stress induced by H2O2

Background Oxidative stress is a main cause of age-related macular degeneration (AMD). Lutein has a preventive role for AMD, but its antioxidant mechanism remains unclear. Objective Present study was to investigate the effect of lutein on oxidative stress of Muller cells and its signaling pathway. Methods Human Muller cells (human Muller cell strain) were cultured, and the cells at logarithmimic growth phase were incubated in 96 well plate overnightly.Oxidative stress cell models were established by adding 160 μmol/L H2O2, a median lethal dose for Muller cells.The models were divided into the model control group and 12.5, 25.0, 50.0 mg/L lutein groups, and the different concentrations of lutein were used to culture the cells for 24 hours, respectively.The routine cultured cells served as the blank control group.Growth of the cells was assayed by MTT method (absorbancy); the reactive oxygen species (ROS) content in the cells was assayed by flow cytometry; the mRNA and protein levels of nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the cells were detected by quantitative real-time PCR and Western blot, respectively. Results The inhibitory effects on the cells were gradually enhanced with the increase of H2O2 concentrations, showing a significant difference among the groups (F=43.890, P<0.01). A significant difference was found in apoptotic rate of the cells among the blank control group, model control group and 12.5, 25.0, 50.0 mg/L lutein groups (F=346.770, P=0.000), and the apoptosis rate was significant elevated with the increase of lutein dose (all at P<0.05). The ROS contents in the cells were 1.92±0.18, 64.89±2.86, 52.70±2.80, 32.61±4.20 and 5.68±1.35 in the blank control group, model control group and 12.5, 25.0, 50.0 mg/L group, respectively, with significant difference among the groups (F=324.900, P=0.000), and the ROS content was gradually reduced as the increase of lutein dose (all at P<0.05). The relative mRNA and protein expressions of Nrf2 and HO-1 were remarkedly higher in the 12.5, 25.0, 50.0 mg/L lutein groups than those in the model control group (F=236.960, 242.620, 186.830, 263.120, all at P=0.000), and no significant difference was seen in the relative expression level of nuclear Nrf2 protein among the groups (F=1.790, P=0.210). Conclusions Lutein can induce the expression of antioxidant enzymes by inducing the expression of nuclear translocation of Nrf2 and consequently inhibit the oxidative stress status. Key words: Oxidative stress/physiology; Lutein/pharmocology; Muller cells; Macular degeneration, age-related; Nuclear factor-E2-related factor 2/metabolism; Heme oxygenase-1/metabolism

Biodegradable Poly (Lactic-co-Glycolic Acid)-Polyethylene Glycol Nanocapsules: An Efficient Carrier for Improved Solubility, Bioavailability, and Anticancer Property of Lutein

Lutein bioavailability is limited because of its poor aqueous solubility. In this study, lutein-poly (lactic-co-glycolic acid) (PLGA)-polyethylene glycol (PEG) nanocapsules were prepared to improve the solubility, bioavailability, and anticancer property of lutein. The scanning electron microscopy and dynamic light scattering examination revealed that the nanocapsules are smooth and spherical with size ranging from 80 to 500 nm (mean = 200 nm). In vitro lutein release profile from nanocapsules showed controlled sustainable release (66%) up to 72 h. Aqueous solubility of lutein nanocapsules was much higher by 735-fold than the lutein. Fourier transform infrared spectroscopy analyses showed no chemical interaction among PLGA, PEG, and lutein, indicating possible weak intermolecular forces like hydrogen bonds. X-ray diffraction revealed lutein is distributed in a disordered amorphous state in nanocapsules. Postprandial plasma kinetics (area under the curve) of an oral dose of lutein from nanocapsules was higher by 5.4-fold compared with that of micellar lutein (control). The antiproliferative effect of lutein from nanocapsules (IC50 value, 10.9 μM) was higher (43.6%) than the lutein (IC50 value, 25 μM). Results suggest that PLGA-PEG nanocapsule is an efficient carrier for enhancing hydrophilicity, bioavailability, and anticancer property of lipophilic molecules such as lutein.

Lutein supplementation leads to decreased soluble complement membrane attack complex sC5b-9 plasma levels.

The purpose of this study was to investigate the effect of lutein on systemic complement activation in elderly individuals. Seventy patients with signs of early age-related macular degeneration (AMD) were included in this study. All subjects were randomly assigned to receive a 10 mg daily dose of lutein or a placebo for a time period of 1 year. EDTA blood was collected before and at various time-points during the study (0, 4, 8 and 12 months). The plasma level of the soluble complement membrane attack complex sC5b-9 was measured by ELISA. We found a significant 1.1 ng/ml monthly decrease in the plasma sC5b-9 concentration in the lutein group (p<0.001), resulting in a decrease from 60.3 ng/ml at baseline to 46.3 ng/ml at 12 months. For the placebo group, we found a significant 0.6 ng/ml monthly increase in plasma sC5b-9 concentration (p=0.001), resulting in an increase from 51.6 ng/ml at baseline to 58.4 ng/ml at 12 months. Lutein supplementation inhibits the systemic activation of the complement system, which provides further functional evidence for the reported beneficial effects of this carotenoid in the management of AMD.

Impact of lutein and docosahexaenoic acid supplementation during lactation on plasma and breast milk (623.18)

We assessed the effect of varying amounts of lutein and docosahexaenoic acid (DHA) on breast milk and plasma levels of these nutrients. Eighty‐eight lactating women 4‐6 weeks post‐partum were randomized in 3 groups: placebo, 6mg of lutein + 200mg DHA (low dose) or 12mg lutein + 400mg DHA (high dose). Breast milk and plasma lutein and DHA were assessed at the beginning and end of the study by HPLC for carotenoids and GC‐FID for fatty acids. Infant plasma lutein and DHA were assessed at the end of the study. Breast milk lutein and DHA were at most 4.5 and 2.2‐fold greater, respectively, as compared to placebo after supplementation; both increased in a dose dependent manner (R2=0.28 lutein; R2=0.20 DHA). Maternal plasma lutein and DHA had a similar fold change, 4.4 and 2.0, respectively, as compared to placebo. Infant plasma lutein was at most 4.2‐fold greater as compared to placebo. Breast milk lutein and DHA were correlated to maternal plasma levels (r=0.7747 lutein; r=0.4994, P&lt;0.0001). Infant plasma lutein was also correlated to breast milk lutein (r=0.8347, P&lt;0.0001) and maternal plasma lutein (r=0.8122, P&lt;0.0001). There was no difference in average dietary intake of lutein or DHA among groups. Our results show that breast milk and plasma are responsive to increasing supplement doses of lutein and DHA and that the variation in these nutrients is also affected by individual variation and responsiveness to supplementation.Grant Funding Source: Supported by Abbott Nutrition

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The present study has been designed to investigate the effect of lutein in streptzotocin induced diabetic nephropathy (DN) in wistar rats. Diabetic nephropathy was induced by administering single dose of streptozotocin in wistar rats. DN was clinically assessed by the estimation of various biochemical parameters and histopathological studies of renal tissue. Diabetic nephropathy was assessed biochemically by blood urea nitrogen, serum creatinine and total urinary protein. Oxidative stress assessed by measuring the Thiobarbituric acid reactive substances (TBARS) level and renal reduced glutathione levels. Treatment with high dose of lutein (1.5 mg/kg, p.o.) shows significant improvement in (blood urea nitrogen (BUN), serum creatinine, total urine protein, ratio of kidney wt/body wt, TBARS, reduced glutathione) renal parameters studied for DN. It may be therefore concluded that renoprotective effect of lutein is due to its antioxidant property. Lutein may prevent overproduction of reactive oxygen species (ROS) and to increase the removal of preformed ROS. This may prove to be effective in preventing the development and progression of diabetic nephropathy. Key words: Diabetic nephropathy, lutein, streptozotocin.