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PubMed1998

Dietary lutein absorption from marigold extract is rapid in BALB/c mice.

Even though lutein can stimulate immunity and decrease cancer growth, no systematic studies are available on the uptake of lutein in mice. We studied the uptake of lutein in 8-wk-old female BALB/c mice fed a diet containing 0, 0.05, 0.1, 0.2 or 0.4% lutein. Mice were killed on d 0, 3, 7, 14, 21 and 28 (n = 6/period), and blood, spleen and liver were collected. Food intake and body, liver and spleen weights did not differ among treatment groups. Lutein + zeaxanthin were not detectable in the plasma, liver and spleen of unsupplemented mice. Mice fed lutein showed very rapid lutein + zeaxanthin absorption. On d 3, concentrations of plasma lutein + zeaxanthin had rapidly increased (P < 0.05) in lutein-fed mice and no further increases were observed. Plasma lutein + zeaxanthin concentrations did not differ among lutein-fed mice by d 7 (2.58 +/- 0.2 micromol/L). Even though maximal uptake of plasma lutein + zeaxanthin was observed by d 3, uptake of lutein + zeaxanthin by the liver and especially by the spleen generally continued to increase (P < 0.05) through d 28 to reach concentrations of 0.11 +/- 0.001 (spleen) and 0.71 +/- 0. 0002 (liver) nmol/g. Therefore, dietary lutein is readily absorbed into the plasma and taken up by liver and spleen of mice. Plasma lutein + zeaxanthin concentrations were higher than in human studies; however, mice were fed lutein at a level several hundredfold greater than in humans. The liver is a major storage organ for lutein + zeaxanthin in mice. Uptake of lutein + zeaxanthin by the spleen suggests a role for lutein in modulating immunity.

Animals↗
PubMed2002

An innovative approach to the determination of safety for a dietary ingredient derived from a new source: case study using a crystalline lutein product.

Lutein and zeaxanthin are antioxidant carotenoids that occur naturally in the diet. A new source of these carotenoids, a crystalline lutein product, is an extract from the marigold flower (Tagetes erecta) that contains approximately 86% by weight of the carotenoids lutein and zeaxanthin. The safety of consumption of a crystalline lutein product used as an ingredient in food is determined by evaluating the safety of ingestion of the whole product, as well as safety of ingestion of the major constituents, lutein and zeaxanthin. The approach to evaluating the safety of increased lutein and zeaxanthin intake from consumption of crystalline lutein product is based on an evaluation of the incremental increase this ingestion will produce in lutein and zeaxanthin and in total carotenoids, compared to background exposure. In addition, bioavailability of lutein+zeaxanthin from crystalline lutein product, when added to food, is determined and used to adjust the estimated daily intake of lutein and zeaxanthin from this new source and standardize it to the bioavailable dose of these carotenoids from food sources. The proposed level of ingestion of lutein and zeaxanthin from the crystalline lutein product would increase intake of lutein zeaxanthin in the generally vegetable-poor American diet to a level comparable to the mean intake of individuals consuming the recommended number of servings of vegetables per day and is therefore determined to be both prudent and safe. Safety of consumption of the whole product is determined by evaluating the source of the product, production process, nature and quantity of impurities, and product specifications. Corroboration of safety is provided by animal toxicology studies of the crystalline lutein product, as well as human and epidemiologic studies of lutein and zeaxanthin intake. It can be concluded that crystalline lutein is a safe and GRAS source of lutein for its proposed uses in food.

Animals↗
PubMed1986

Absorption, transport, and deposition in chickens of lutein diester, a carotenoid extracted from marigold (Tagetes erecta) petals.

Young broiler chickens were fed from hatching until 3 weeks of age with a white corn-soy diet amended with varying amounts of lutein diester to supply 0, 5, 10, 20, 40, and 80 micrograms free lutein/g diet. The lutein diester was added as a stabilized, microencapsulated extract of marigold (Tagetes erecta) petals. The concentrations of lutein diester, lutein monoester, and lutein in the contents of the jejunum and large intestine and in serum, liver, and toe web from these birds were measured by high pressure liquid chromatography. The contents of the jejunum and large intestine contained a mixture of lutein diester, lutein monoester, and lutein. The serum contained lutein (approximately 90%), lutein monoester (approximately 10%), and traces of lutein diester. The liver contained the three carotenoid classes in ratios reflecting the serum ratios. The ratios in toe web, an integumentary depot site, were reversed with lutein diester much greater than lutein monoester greater than lutein. The concentrations of each class in each tissue bore a linear relationship to the concentration of lutein diester in the diet. A simple explanation for these data is that the dietary lutein diester was hydrolyzed mainly to lutein, which was absorbed through the intestinal wall into the blood stream where it was transported to the liver, a storage site, and to the integumentary sites where it is esterified to lutein diester which is the main depot form.

Animals↗
PubMed2005

Lutein: a valuable ingredient of fruit and vegetables.

Lutein is a human serum carotenoid which is not synthesized by humans and thus must be obtained by the ingestion of food containing it such as fruits and vegetables. Lutein is present in different forms in those foods as all-trans-lutein, cis-lutein, epoxi-lutein, and lutein linked to proteins. It discusses if the intake of lutein or diets supplemented with lutein or diets rich in fruits and vegetables are important in the prevention of diseases like some cancers, cardiovascular diseases, etc., that may be affected by the antioxidant effect of lutein; or in the prevention of age-related macular degeneration and other eye diseases. The concentration of lutein in fruits and vegetables depends on the species. We've included the concentration of lutein in 74 species reported by different authors since 1990. Currently the quantification of lutein is mainly performed by HPLC, but more investigations into a quantification method for lutein, lutein isomers, and epoxi-lutein are necessary. Improvement of lutein extraction methods is important as well. Methods commonly used in the vegetable and fruit industry like heat treatment, storage conditions, etc. can change lutein concentrations; other factors depend on the plant, for instance the variety, the stage of maturity, etc.

Biological Availability↗
PubMed2002

Esterification does not impair lutein bioavailability in humans.

Age-related macular degeneration (ARMD) is inversely associated with the accumulation of lutein + zeaxanthin in the macula, but higher lutein intakes are inconsistently related to reduced risk of ARMD in epidemiologic studies. Resolution of efficacy awaits clinical trials designed with knowledge of lutein supplement pharmacokinetics. Lutein bioavailability was determined for lutein diester and unesterified lutein formulations as they might be incorporated into dietary supplements. Healthy subjects (n = 18) consumed a single dose of each formulation (either 0.5 or 0.67 micro mol lutein/kg body, 10 and 8 subjects, respectively) in random order, and the appearance of free lutein + zeaxanthin was measured in serum from 0 to 408 h. Areas under the serum concentration x time curves (AUC), as a measure of bioavailability, were independent of gender, body mass index and lutein dose. The lutein diester formulation was 61.6% more bioavailable than the unesterified lutein formulation with higher mean AUC, maximum serum concentration and ascending slope (P < 0.05). The AUC was greater in 14 of 18 subjects when they consumed the lutein diester formulation. Comparison with data from previous studies suggested that dissolution was a greater limitation to bioavailability than lutein ester hydrolysis because an oil-solubilized unesterified lutein preparation, given at 0.5 micro mol/kg body, resulted in greater mean peak concentrations and AUC compared with either the unesterified or lutein diester formulations used in our study. In conclusion, the lutein diester formulation poses no impediment to lutein bioavailability at the doses tested, but formulation dissolution is an important factor in lutein bioavailability and should be evaluated before a supplement and dose are selected for use in clinical trials.

Adult↗
PubMed1987

Metabolism of lutein diester during aflatoxicosis in young chickens.

Young chickens were fed from hatching until 3 wk of age with a white corn-soy diet amended with lutein diester to supply 25 micrograms lutein/g diet and with varying amounts of aflatoxin (0, 1, 2, 4, and 8 micrograms/g diet). The lutein diester was added as a stabilized, microencapsulated extract of marigold (Tagetes erecta) petals. Aflatoxin had no significant effect on the partial conversion of lutein diester to lutein monoester and lutein that occurs in the jejunum of normal chickens. The concentration of lutein in the jejunal mucosa was increased slightly by intermediate levels of aflatoxin and depressed by higher levels. Aflatoxin depressed lutein (the dominant form) in serum by up to 40%. Aflatoxin enhanced the lutein accumulation in the liver as the monoester (four-fold) and diester (12-fold). Only minor effects of aflatoxin on the carotenoid content of the toe webs were noted in birds fed lutein diester. These results imply that the main effects of aflatoxin on the utilization of lutein diester are to impair the absorption of lutein, which is an intestinal product of dietary lutein diester, and to sequester lutein as lutein monoester and lutein diester in the liver.

Animals↗
PubMed1986

Modulation of luteinizing hormone immunoreactivity and bioactivity by dopamine but not norepinephrine in women.

It has been suggested that changes in bioactive luteinizing hormone in women occur toward midcycle and may result in increased bioactive/immunoreactive luteinizing hormone ratios. To determine whether dopamine or norepinephrine modulate immunoreactive and bioactive luteinizing hormone secretion, 15 ovulatory women were studied in the mid to late follicular phase. Dopamine in two doses (0.5 micrograms/kg/min and 4 micrograms/kg/min) and norepinephrine, 0.1 microgram/kg/min, were infused for 4 hours, and metoclopramide, 10 mg intravenously, was also given to determine whether dopamine receptor antagonism results in changes. Bioactive luteinizing hormone and the bioactive/immunoreactive luteinizing hormone ratio increased in women from the early to late follicular phase (p less than 0.05). Both intravenous doses of dopamine resulted in significant decrements in immunoreactive luteinizing hormone (20 +/- 2 and 20 +/- 3%, p less than 0.02) and bioactive luteinizing hormone (36.7% and 43.2%, p less than 0.05). With dopamine there was also a significant decrease in the bioactive/immunoreactive luteinizing hormone ratio (p less than 0.02). Intravenous norepinephrine, however, resulted in no changes in either immunoreactive or bioactive luteinizing hormone levels. Metoclopramide also did not change immunoreactive or bioactive luteinizing hormone levels. These data suggest that although endogenous dopaminergic blockade may not play a significant role in determining basal levels of luteinizing hormone, decreases in dopamine at the pituitary level may increase the bioactive/immunoreactive luteinizing hormone ratio. Norepinephrine does not appear to exert major changes in immunoreactive or bioactive luteinizing hormone.

Adult↗
PubMed2004

The science behind lutein.

In humans, as in plants, the xanthophyll lutein is believed to function in two important ways: first as a filter of high energy blue light, and second as an antioxidant that quenches and scavenges photo induced reactive oxygen species (ROS). Evidence suggests that lutein consumption is inversely related to eye diseases such as age-related macular degeneration (AMD) and cataracts. This is supported by the finding that lutein (and a stereo isomer, zeaxanthin) are deposited in the lens and the macula lutea, an area of the retina responsible for central and high acuity vision. Human intervention studies show that lutein supplementation results in increased macular pigment and improved vision in patients with AMD and other ocular diseases. Lutein may also serve to protect skin from UV-induced damage and may help reduce the risk of cardiovascular disease. Crystalline lutein is readily absorbed from foods and from dietary supplements whereas, to enter the bloodstream, lutein esters require prior de-esterification by intestinal enzymes. Unlike the hydrocarbon carotenoids which are mainly found in the LDL fraction, xanthophylls like lutein and zeaxanthin are incorporated into both HDL and LDL. Today, lutein can be obtained from the diet in several different ways, including via supplements, and most recently in functional foods. Animal toxicology studies have been performed to established lutein's safety as a nutrient. These studies have contributed to the classification of purified crystalline lutein as generally recognized as safe (GRAS). The achievement of GRAS status for purified crystalline lutein allows for the addition of this form into several food and beverage applications. This achievement speaks directly to the quality and safety of purified lutein.

Animals↗
PubMed2000

Relation among serum and tissue concentrations of lutein and zeaxanthin and macular pigment density.

BACKGROUND: Lutein and zeaxanthin are the only carotenoids in the macular region of the retina (referred to as macular pigment [MP]). Foods that are rich in lutein and zeaxanthin can increase MP density. Response to dietary lutein and zeaxanthin in other tissues has not been studied. OBJECTIVE: The objective of this study was to examine tissue responses to dietary lutein and zeaxanthin and relations among tissues in lutein and zeaxanthin concentrations. DESIGN: Seven subjects consumed spinach and corn, which contain lutein and zeaxanthin, with their daily diets for 15 wk. At 0, 4, 8, and 15 wk and 2 mo after the study, serum, buccal mucosa cells, and adipose tissue were analyzed for carotenoids, and MP density was measured. RESULTS: Serum and buccal cell concentrations of lutein increased significantly from baseline during dietary modification. Serum zeaxanthin concentrations were greater than at baseline only at 4 wk, whereas buccal cell and adipose tissue concentrations of zeaxanthin did not change. Adipose tissue lutein concentrations peaked at 8 wk. Changes in adipose tissue lutein concentration were inversely related to the changes in MP density, suggesting an interaction between adipose tissue and retina in lutein metabolism. To investigate the possibility of tissue interactions, we examined cross-sectional relations among serum, tissue, and dietary lutein concentrations, anthropometric measures, and MP density in healthy adults. Significant negative correlations were found between adipose tissue lutein concentrations and MP for women, but a significant positive relation was found for men. CONCLUSION: Sex differences in lutein metabolism may be an important factor in tissue interactions and in determining MP density.

Adipose Tissue↗
PubMed1999

Lutein and zeaxanthin as protectors of lipid membranes against oxidative damage: the structural aspects.

Two main xanthophyll pigments are present in the membranes of macula lutea of the vision apparatus of primates, including humans: lutein and zeaxanthin. Protection against oxidative damage of the lipid matrix and screening against excess radiation are the most likely physiological functions of these xanthophyll pigments in macular membranes. A protective effect of lutein and zeaxanthin against oxidative damage of egg yolk lecithin liposomal membranes induced by exposure to UV radiation and incubation with 2, 2'-azobis(2-methypropionamidine)dihydrochloride, a water-soluble peroxidation initiator, was studied. Both lutein and zeaxanthin were found to protect lipid membranes against free radical attack with almost the same efficacy. The UV-induced lipid oxidation was also slowed down by lutein and zeaxanthin to a very similar rate in the initial stage of the experiments (5-15 min illumination) but zeaxanthin appeared to be a better photoprotector during the prolonged UV exposure. The decrease in time of a protective efficacy of lutein was attributed to the photooxidation of the carotenoid itself. Both lutein and zeaxanthin were found to slightly modify mechanical properties of the liposomes in a very similar fashion as concluded on the basis of H(1) NMR and diffractometric measurements of pure egg yolk membranes and membranes pigmented with the xanthophylls. Linear dichroism analysis of the mean orientation of the dipole transition moment of the xanthophylls incorporated to the lipid multibilayers revealed essentially different orientation of zeaxanthin and lutein in the membranes. Zeaxanthin was found to adopt roughly vertical orientation with respect to the plane of the membrane. The relatively large orientation angle between the transition dipole and the axis normal to the plane of the membrane found in the case of lutein (67 degrees in the case of 2 mol% lutein in EYPC membranes) was interpreted as a representation of the existence of two orthogonally oriented pools of lutein, one following the orientation of zeaxanthin and the second parallel with respect to the plane of the membrane. The differences in the protective efficacy of lutein and zeaxanthin in lipid membranes were attributed to a different organization of zeaxanthin-lipid and lutein-lipid membranes.

Antioxidants↗
PubMed2006

Enhanced lutein bioavailability by lyso-phosphatidylcholine in rats.

The bioavailability of lutein solubilized in mixed micelles containing either phosphatidylcholine (PC) or lysophosphatidylcholine (lysoPC) was evaluated in male rats. Mixed micelles contained 2.5 mM monooleoylglycerol, 7.5 mM oleic acid, 12 mM sodium taurocholate and 200 microM lutein either with 3 mM PC or lysoPC. To study lutein bioavailability, single and repeated dose experiments were conducted. For single dose study, group of rats (n = 30/group) were fed single dose of lutein solubilized in lysoPC (LPC group), PC (PC group) and no phospholipids (NoPL group) in micellar form. Each group was further divided in to five sub-groups (n = 6/sub group) to measure lutein bioavailability over time up to 9 h. For repeated dose study, group of rats (n = 6/group) were fed daily for 10 days a dose of lutein in mixed micelles with NoPL, PC and LPC. A separate group (n = 6) not fed mixed micelles was considered as zero-time control. In both the experiments, mixed micelles (0.2 ml/rat) were fed to the rat by direct intubation to the stomach. Results of single dose studies showed that the mean lutein levels in the plasma and liver of the PC group was significantly lower (p < 0.05) than those of the other two groups. Moreover, the average lutein level in the plasma and liver was significantly (p < 0.05) different among the groups in the order LPC > NoPL > PC. But, repeated dose experiment followed the order LPC > PC > NoPL. The level of lutein excreted through urine and feces of PC group was significantly higher (p < 0.05) than those of the other two groups. Thus, the results indicate that the PC in the mixed micelles suppressed the intestinal uptake of lutein after single dose but not after repeated dose and that lysoPC enhanced the absorption. In both the experiments, plasma and liver level of lutein was higher in LPC compared with PC group. Results also suggest that the luminal hydrolysis of PC to lysoPC is necessary for intestinal uptake of lutein solubilized in mixed micelles.

Animals↗
PubMed2007

The selective retention of lutein, meso-zeaxanthin and zeaxanthin in the retina of chicks fed a xanthophyll-free diet.

Lutein and zeaxanthin are pigmented oxygenated carotenoids, or xanthophylls, derived from plants and concentrated in the retina of primates and birds. We investigated the transport, distribution and depletion of lutein and zeaxanthin in the plasma and tissues of newly hatched chicks fed xanthophyll-free diets. One-day-old Leghorn chicks were randomly divided into two groups. A control group was fed a diet containing lutein and zeaxanthin (5.2 and 1.7 mg/kg diet, respectively) for 28 days. An experimental group was fed a diet containing no lutein and zeaxanthin for 28 days. Plasma and tissues were analyzed for lutein and zeaxanthin at 28 days (control) and on days 1, 14 and 28 (experimental). At hatching, lutein and zeaxanthin were the predominant carotenoids present in the blood and tissues. As indicated by their similar mass contents, there was complete transfer of these carotenoids from egg yolk to chick. Lutein and zeaxanthin concentrations in the plasma and tissues of chicks fed the xanthophyll-free diet decreased rapidly to almost zero (with a depletion time of seven days [t(1/2)]). In contrast, the retina retained its initial concentrations of lutein and zeaxanthin similar to the control group. meso-Zeaxanthin and cis-zeaxanthin were identified only in the retina. The retina concentrated zeaxanthin over lutein. Lutein and zeaxanthin were selectively retained in the retinas of chicks fed a xanthophyll-free diet. In contrast, the plasma and other tissues lost up to 90% of their original content of xanthophylls. These data emphasize the relative stability of lutein and zeaxanthin in the cone-rich retina where they are present as esters in oil droplets. The tissue depletion suggests the need for a regular dietary intake of lutein and zeaxanthin because of rapid depletion in the body. It is clear that these xanthophylls may have an essential role in the cone-rich retina of the chick as evidenced by their selective retention.

Animals↗
PubMed2006

Inhibition of nNOS and COX-2 expression by lutein in acute retinal ischemia.

OBJECTIVE: Lutein is a major nutrient in the retina. Lutein has an antioxidative effect and protects against macular degeneration and retinal degenerative disease. However, the mechanism of lutein is not clear in retinal degeneration, and a role for lutein is not known in ischemic injury. In this study, an ischemia-induced rat retina was examined to determine the effect of the lutein on ischemic retinal cell death. METHODS: We used a transient ischemia model of high intraocular pressure in the rat. Lutein (Kemin Foods, LC) was injected into the intraperitoneal or intravitreous before ischemia. Retinal degeneration was observed by light microscopy 24 h after ischemia. Expressions of neuronal nitric oxide synthase (nNOS) and cyclo-oxygenase-2 (COX-2) were detected by western blot analysis at various times after retinal ischemia. RESULTS: The nNOS and COX-2 expression levels were increased early in ischemic control retinas, but these increases were inhibited by lutein. In addition, the inhibitory effect of lutein was observed to be dose dependent. Further, ischemia-induced cell death was inhibited by lutein. Lutein-injected ischemic retina appeared similar to normal retina. CONCLUSION: This study investigated the protective effect of lutein on retinal ischemia and the inhibitory effect of nNOS and COX-2 expressions. These results suggest that a supplement with lutein may have the potential to inhibit ischemic cell death by this mechanism in the neural retina.

Acute Disease↗
PubMed2005

Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI).

The carotenoid lutein is thought to play a role in the human eye and to protect against age-related macular degeneration. Lutein transport in the human intestine has not been characterized. We examined lutein transport processes using Caco-2 TC-7 monolayers as a model for human intestinal epithelium. Purified lutein was mixed with phospholipids, lysophospholipids, cholesterol, mono-olein, oleic acid and taurocholate to obtain lutein-rich mixed micelles that mimicked those found under physiological conditions. The micelles were added to the apical side of Caco-2 TC-7 cell monolayers for 30 min or 3 h at 37 degrees C. Absorbed lutein, i.e. the sum of lutein recovered in the scraped cells and in the basolateral chamber, was quantified by HPLC. Transport rate was measured (i) as a function of time (from 15 to 60 min), (ii) as a function of micellar lutein concentration (from 1.5 to 15 microM), (iii) at 4 degrees C, (iv) in the basolateral to apical direction, (v) after trypsin pretreatment, (vi) in the presence of beta-carotene and/or lycopene, (vii) in the presence of increasing concentrations of antibody against SR-BI (scavenger receptor class B type 1) and (viii) in the presence of increasing concentrations of a chemical inhibitor of the selective transfer of lipids mediated by SR-BI, i.e. BLT1 (blocks lipid transport 1). The rate of transport of lutein as a function of time and as a function of concentration was saturable. It was significantly lower at 4 degrees C than at 37 degrees C (approx. 50%), in the basal to apical direction than in the opposite direction (approx. 85%), and after trypsin pretreatment (up to 45%). Co-incubation with beta-carotene, but not lycopene, decreased the lutein absorption rate (approx. 20%) significantly. Anti-SR-BI antibody and BLT1 significantly impaired the absorption rate (approx. 30% and 57% respectively). Overall, these results indicate that lutein absorption is, at least partly, protein-mediated and that some lutein is taken up through SR-BI.

Binding, Competitive↗
PubMed1983

Action of luteinizing hormone-releasing hormone: involvement of novel arachidonic acid metabolites.

Anterior pituitary cells were incubated in the presence of luteinizing hormone-releasing hormone and one of three inhibitors of arachidonic acid metabolism:indomethacin, an inhibitor of the cyclooxygenase system; nordihydroguaiaretic acid, an antioxidant that inhibits lipoxygenase; and icosatetraynoic acid, an acetylenic analogue of arachidonic acid that blocks all known pathways of arachidonic acid metabolism. Indomethacin was ineffective in blocking luteinizing hormone-releasing hormone-stimulated luteinizing hormone secretion. Nordihydroguaiaretic acid was only marginally capable of inhibiting luteinizing hormone-releasing hormone-stimulated luteinizing hormone secretion. Icosatetraynoic acid at 10 microM completely inhibited stimulated luteinizing hormone secretion. Addition of several epoxygenated arachidonic acid metabolites to cells in vitro resulted in secretion of luteinizing hormone equal to or greater than that induced by 10 nM luteinizing hormone-releasing hormone. The half-maximal effective dose for these compounds was approximately 50 nM. The 5,6-epoxyicosatrienoic acid was the most potent of the compounds tested. These studies suggest that luteinizing hormone-releasing hormone-stimulated luteinizing hormone release is closely coupled with the production of oxidized arachidonic acid metabolites. Moreover, one or more of the epoxygenated arachidonic acid metabolites might be a component of the cascade of reactions initiated by luteinizing hormone-releasing hormone that ultimately results in secretion of luteinizing hormone.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed2006

Lutein and eicosapentaenoic acid interact to modify iNOS mRNA levels through the PPARgamma/RXR pathway in chickens and HD11 cell lines.

Two experiments were conducted to investigate the effect of lutein and fat or eicosapentaenoic acid (EPA) interaction on inducible nitric oxide synthase (iNOS), PPARs alpha, beta, and gamma, and retinoic acid X receptor (RXR) alpha and gamma mRNA levels. In Expt. 1, macrophages were collected from broiler chicks fed 3 or 6% dietary fat (g/100 g) with 0, 25, and 50 mg lutein/kg feed for 23 d. In Expt. 2, using a 3 x 3 factorial, eicosapentaenoic acid (EPA) at 0, 15 and 50 micromol/L and lutein at 0, 10 and 100 micromol/L were applied to HD11 cell culture for 24 h. In both experiments, cells were stimulated with lipopolysaccharide before RNA isolation. Lutein interacted with fat in Expt. 1 and with EPA in Expt. 2 to affect mRNA levels of iNOS, PPARgamma, and RXRalpha in chicken macrophages and HD11 cells, respectively (P < 0.05). At 3% dietary fat or up to 15 micromol/L EPA in the medium, increasing lutein increased the iNOS mRNA. However, at 6% dietary fat or 50 micromol/L EPA, lutein did not cause a rise in iNOS mRNA. Increasing lutein in the medium from 0 to 100 micromol/L decreased iNOS mRNA. Increasing lutein with high fat (6%) or EPA (15 micromol/L EPA) increased PPARgamma and RXRalpha mRNA levels. Lutein increased PPARalpha mRNA levels in both macrophages (P < 0.01) and HD11 (P = 0.01) cells and RXRgamma (P < 0.01) mRNA levels in macrophages. GW9662, a PPARgamma antagonist, prevented (P < 0.01) the lutein-induced iNOS mRNA downregulation in HD11 cells. LG101208, a RXR antagonist, prevented (P < 0.01) iNOS upregulation induced by 10 micromol/L lutein and iNOS mRNA downregulation induced by 100 micromol/L lutein. We conclude that lutein and EPA interact through the PPARgamma and RXR pathways to modulate iNOS mRNA.

Anilides↗
PubMed2004

Enrichment of eggs with lutein.

Lutein is being considered as a nutrient for prevention of macular degeneration in the aging population. Two experiments were designed to study the transfer efficiency of lutein from the layers' diet into the egg. In experiment 1, laying hens were fed corn-soy diets supplemented with 0, 125, 250, 375, 500, 625, 750, or 1000 ppm of lutein. After 30 d, eggs were collected and assayed for lutein. In a second study, layers were fed corn-soy diets or diets containing corn gluten meal and alfalfa, with or without added flaxseed. Diets in experiment 2 were supplemented with 0, 125, 250, or 500 ppm of lutein. Adding lutein to the layers' diet resulted in a significant (P < 0.01) increase in Roche color score of yolk within 7 d of supplementation. In experiment 1, lutein was transferred into the yolk (P < 0.01) increasing from a basal level of 0.3 mg to 1.5 mg/60 g of egg. However, there was no significant (P > 0.05) increase in yolk lutein with diet supplements >375 ppm. In the second experiment, using corn gluten meal and alfalfa further increased lutein content that leveled off at 2.2 mg/60 g of egg with a diet supplement of 500 ppm of lutein. Adding flax to these diets seemed to depress yolk lutein content. Yolk lutein content can be increased, although further studies are needed to investigate the major decline in transfer efficiency seen with higher levels of dietary supplementation.

Animal Feed↗
PubMedDate not supplied

Dietary lutein inhibits mouse mammary tumor growth by regulating angiogenesis and apoptosis.

Even though we previously reported that dietary lutein can inhibit mammary tumor growth, the mechanism of this action was unknown. Here, we studied the action of dietary lutein through its possible regulation of apoptosis and angiogenesis. Female BALB/c mice were fed a semi-purified diet containing 0 (control), 0.002 or 0.02% lutein (n = 20/treatment) for 2 weeks prior to inoculation with 100,000 -SA mouse mammary tumor cells into the right mammary fat pad. Tumor volume was measured daily until day 50 postinoculation when all mice were killed. Angiogenesis and apoptosis activities in the tumors were measured by immunohistochemistry. Apoptosis and necrosis of blood lymphocytes were quantitated by flow cytometry using Annexin V-FITC and propidium iodide staining. The expression of the p53, Bax and Bcl-2 mRNA was measured by RT-PCR amplification. Lutein was not detectable in the plasma, liver or tumor of unsupplemented mice, but increased in a dose-dependent manner in lutein-supplemented mice. Mice fed lutein had tumors that were 30 to 40% smaller (p < 0.05) on day 50 post-inoculation compared to unsupplemented mice. Final tumor volume was lowest in mice fed 0.002% lutein. Mice fed lutein had higher apoptotic activity in the tumors but lower apoptotic activity in blood lymphocytes as compared to unsupplemented animals. These observations were supported by the observed increase in the expression of the proapoptotic genes, p53 and Bax, together with a decrease in the expression of the antiapoptotic gene, Bcl-2, and consequently an increase in the Bax:Bcl-2 ratio in tumors from lutein-fed mice. Furthermore, lutein-fed mice also had lower (p < 0.05) angiogenic activity in the tumors as compared to unsupplemented mice. The greatest beneficial effect on apoptosis and angiogenesis was observed with mice fed 0.002% lutein. Therefore, dietary lutein, especially at 0.002%, inhibited tumor growth by selectively modulating apoptosis, and by inhibiting angiogenesis.

Animals↗