Dietary Lutein Research Articles

Lutein Interacts with Ascorbic Acid More Frequently than with α-Tocopherol to Alter Biomarkers of Oxidative Stress in Female Zucker Obese Rats

The influence of dietary lutein, with and without moderate amounts of vitamin C (VC) or vitamin E (VE), on biomarkers of oxidative stress was examined in rats. Nine groups of immature Zucker obese (fa/fa) and lean female rats (8/group) consumed ad libitum for 8 wk the AIN-93G diet (Control) to which was added either dl-alpha-tocopherol acetate (VE) at 0.60 mg/kg or ascorbic acid (VC) at 0.75 mg/kg diet. Each of these diets contained lutein oil (FloraGlo) at 0.5 (Lut0.5) or 1.0 (Lut1.0) mg/kg diet. Weight gain, food efficiency and relative liver weight were higher in obese than in lean rats. Although liver malondialdehyde (MDA) concentrations were significantly higher in obese than in lean rats, levels were significantly lower in obese rats fed VE, VE-Lut and VC-Lut0.5 compared with other obese groups. The accumulation of alpha-tocopherol in liver was 6- and 3-times greater in the VE and VE-Lut1.0 groups, respectively, compared with the obese and lean control groups. Lutein reduced the activity of superoxide dismutase (SOD) in obese rats, independent of VC or VE, and raised the activity of glutathione peroxidase to higher levels in lean rats when combined with VC. Plasma insulin levels were dramatically higher in obese compared with lean rats, but significantly lower in obese rats fed VC-Lut0.5, VE-Lut1.0 and Lut1.0 compared with the Control group. These results suggest that lutein independently reduces the activity of SOD and alters more biomarkers of oxidative stress when combined with vitamin C than with vitamin E, and that vitamin E reduces liver lipid peroxidation in obese rats when the accumulation of liver alpha-tocopherol is very high.

Dietary Lutein/Zeaxanthin Decreases Ultraviolet B-Induced Epidermal Hyperproliferation and Acute Inflammation in Hairless Mice

Lutein and zeaxanthin are carotenoids found in green leafy vegetables with interesting antioxidant properties. They are present in high concentrations in the fovea centralis of the human retina and their role in the prevention of age-related macula degeneration has been reported. We have investigated the effect of orally administered lutein and zeaxanthin in the cutaneous response to ultraviolet B irradiation. Female hairless SKh-1 mice receiving 0.4% and 0.04% lutein plus zeaxanthin-enriched diet for 2 wk were exposed to single doses of ultraviolet B radiation. Skin biopsies were taken at 24 and 48 h after irradiation and analyzed for the presence of apoptotic cells, proliferating cells, and expression of proliferating cell nuclear antigen. Our results show a clear ultraviolet-induced dose-dependent inflammatory response. Orally administered 0.4% lutein and zeaxanthin decreased significantly the edematous cutaneous response (p<0.01) as determined by the reduction of the UVB-induced increase of ear bifold thickening. Additionally, dietary carotenoids were efficient in reducing the ultraviolet B-induced increases in the percentage of proliferating cell nuclear antigen (p<0.05), bromodeoxyuridine (p<0.05), and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling-positive cells (p<0.01). These data demonstrate that oral supplementation of lutein and zeaxanthin diminishes the effects of ultraviolet B irradiation by reducing acute inflammatory responses and ultraviolet-induced hyperproliferative rebound.

Lutein-based plumage coloration in songbirds is a consequence of selective pigment incorporation into feathers

Many birds obtain colorful carotenoid pigments from the diet and deposit them into growing tissues to develop extravagant red, orange or yellow sexual ornaments. In these instances, it is often unclear whether all dietary pigments are used as integumentary colorants or whether certain carotenoids are preferentially excluded or incorporated into tissues. We examined the carotenoid profiles of three New World passerines that display yellow plumage coloration—the yellow warbler ( Dendroica petechia), common yellowthroat ( Geothlypis trichas) and evening grosbeak ( Coccothraustes vespertinus). Using high-performance liquid chromatography, we found that all species used only one carotenoid—lutein—to color their plumage yellow. Analyses of blood carotenoids (which document those pigments taken up from the diet) in two of the species, however, revealed the presence of two dietary xanthophylls—lutein and zeaxanthin—that commonly co-occur in plants and animals. These findings demonstrate post-absorptive selectivity of carotenoid deposition in bird feathers. To learn more about the site of pigment discrimination, we also analyzed the carotenoid composition of lipid fractions from the follicles of immature yellow-pigmented feathers in G. trichas and D. petechia and again detected both lutein and zeaxanthin. This suggests that selective lutein incorporation in feathers is under local control at the maturing feather follicle.

The effect of an acute phase response on tissue carotenoid levels of growing chickens ( Gallus gallus domesticus)

Plasma, liver and skin carotenoids decrease following infectious disease challenges. Since these challenges often involve substantial host pathology and chronic immune responses, the mechanism underlying altered carotenoid deposition is unclear. Therefore, changes in tissue carotenoid levels were examined during an acute phase response induced by lipopolysaccharide (LPS) or interleukin-1 (IL-1). In two experiments, chicks were hatched from carotenoid-deplete eggs ( n=28, n=64, respectively) and fed 0, 8 or 38 mg carotenoids (lutein+canthaxanthin)/kg diet. For chicks fed 38 mg carotenoids, but not those fed 0 or 8 mg, LPS generally reduced plasma lutein, canthaxanthin and total carotenoids ( P<0.05), and liver lutein, zeaxanthin, canthaxanthin and total carotenoids ( P<0.05). Additionally, LPS reduced thymic total carotenoids ( P=0.05) and increased thymocyte lutein ( P=0.07), zeaxanthin ( P=0.07) and total carotenoids ( P=0.07). Finally, LPS increased bursal canthaxanthin ( P<0.01), but had no effect on shank carotenoids ( P>0.5). In chicks hatched from carotenoid-replete eggs ( n=36) and fed dietary lutein (38 mg/kg diet), LPS reduced plasma and liver zeaxanthin and liver total carotenoids ( P<0.05); IL-1 reduced plasma and liver lutein, zeaxanthin and total carotenoids ( P<0.05). Therefore, an acute phase response plays a role in reduced tissue carotenoids during infectious disease.

Biologic mechanisms of the protective role of lutein and zeaxanthin in the eye.

The macular region of the primate retina is yellow in color due to the presence of the macular pigment, composed of two dietary xanthophylls, lutein and zeaxanthin, and another xanthophyll, meso-zeaxanthin. The latter is presumably formed from either lutein or zeaxanthin in the retina. By absorbing blue-light, the macular pigment protects the underlying photoreceptor cell layer from light damage, possibly initiated by the formation of reactive oxygen species during a photosensitized reaction. There is ample epidemiological evidence that the amount of macular pigment is inversely associated with the incidence of age-related macular degeneration, an irreversible process that is the major cause of blindness in the elderly. The macular pigment can be increased in primates by either increasing the intake of foods that are rich in lutein and zeaxanthin, such as dark-green leafy vegetables, or by supplementation with lutein or zeaxanthin. Although increasing the intake of lutein or zeaxanthin might prove to be protective against the development of age-related macular degeneration, a causative relationship has yet to be experimentally demonstrated.

Diet and Lifestyle Correlates of Lutein in the Blood and Diet

Observational studies have suggested an inverse relationship between dietary or serum lutein and risk for age-related macular degeneration and cataracts. This evidence has stimulated interest in the biological and other characteristics of lutein, and also zeaxanthin, a structurally similar carotenoid; together, they comprise the macular pigment. Accurate interpretation of data linking dietary intake or serum concentrations of lutein and zeaxanthin and risk for eye disease in epidemiologic and clinical studies requires knowledge of biological and nondietary factors influencing these intake data or concentrations. The primary aims of this study were to identify the correlates of dietary lutein + zeaxanthin intake and the determinants of serum lutein and zeaxanthin concentrations in a heterogeneous community-based sample of adults aged 18-92 y, recruited and examined at three U.S. sites (n = 2786). An additional aim was to identify the determinants of change in serum lutein concentration from baseline to 1 y in a subset of 1368 study participants followed prospectively. Demographic characteristics (age, sex, race/ethnicity, education), body mass index and lifestyle factors (exercise, sun exposure, smoking, alcohol consumption) were significantly (P < 0.05) associated with dietary lutein + zeaxanthin intake. Demographic characteristics, dietary intake, serum cholesterol concentration, body mass index and smoking explained 24% of the variance in serum lutein concentration. Race/ethnicity, education level and smoking had the strongest associations with serum lutein concentration. Every 10% increase in dietary lutein + zeaxanthin intake was associated with a 2.4% increase in serum lutein concentration. Notably, however, the amount of variance in serum concentration that is explained by demographic characteristics, health-related behaviors and lifestyle factors remains substantial.

Relation between dietary intake, serum concentrations, and retinal concentrations of lutein and zeaxanthin in adults in a Midwest population

Information on concentrations of retinal carotenoids (macular pigment, or MP) is of particular interest because MP protects against age-related macular degeneration, the leading cause of irreversible blindness in the United States. This study was designed to evaluate the relation between dietary intake, blood concentrations, and retinal concentrations of carotenoids in a large group of volunteers. Two hundred eighty volunteers in the Indianapolis area completed health and diet questionnaires, donated a blood sample, and participated in MP density assessment to determine retinal carotenoid status. Dietary intake was assessed by food-frequency questionnaire. Serum concentrations of lutein, zeaxanthin, and beta-carotene were measured by HPLC. MP optical density (MPOD) was determined psychophysically with a 460-nm, 1 degrees test stimulus. Average MPOD was 0.21 +/- 0.13. Average intakes of lutein + zeaxanthin and beta-carotene were 1101 +/- 838 and 2935 +/- 2698 microg/d, respectively. Although several key dietary intake variables (eg, lutein + zeaxanthin and beta-carotene) differed by sex, no significant sex differences were found in either serum concentrations of lutein and zeaxanthin or MPOD. Serum beta-carotene concentrations were significantly higher in women than in men. Serum lutein + zeaxanthin and dietary intake of lutein + zeaxanthin were significantly correlated and significantly related to variations in MPOD (r = 0.21, P < 0.001, and r = 0.25, P < 0.001, respectively). Retinal carotenoids can be measured in epidemiologic studies. In this study, MPOD was associated with lutein + zeaxanthin in the diet and the serum. Retinal concentrations, however, were influenced by other factors as well. To understand the effect of dietary lutein + zeaxanthin intake on the retina and risk of age-related eye disease, future studies should include measures of macular concentrations of these pigments.

The Potential Role of Dietary Xanthophylls in Cataract and Age-Related Macular Degeneration

The carotenoid xanthophylls, lutein and zeaxanthin, accumulate in the eye lens and macular region of the retina. Lutein and zeaxanthin concentrations in the macula are greater than those found in plasma and other tissues. A relationship between macular pigment optical density, a marker of lutein and zeaxanthin concentration in the macula, and lens optical density, an antecedent of cataractous changes, has been suggested. The xanthophylls may act to protect the eye from ultraviolet phototoxicity via quenching reactive oxygen species and/or other mechanisms. Some observational studies have shown that generous intakes of lutein and zeaxanthin, particularly from certain xanthophyll-rich foods like spinach, broccoli and eggs, are associated with a significant reduction in the risk for cataract (up to 20%) and for age-related macular degeneration (up to 40%). While the pathophysiology of cataract and age-related macular degeneration is complex and contains both environmental and genetic components, research studies suggest dietary factors including antioxidant vitamins and xanthophylls may contribute to a reduction in the risk of these degenerative eye diseases. Further research is necessary to confirm these observations.

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

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. The objective of this study was to examine tissue responses to dietary lutein and zeaxanthin and relations among tissues in lutein and zeaxanthin concentrations. 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. 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. Sex differences in lutein metabolism may be an important factor in tissue interactions and in determining MP density.

Dietary lutein stimulates immune response in the canine

The possible immuno-modulatory action of dietary lutein in dogs is not known. Female Beagle dogs (17–18-month old; 11.4±0.4 kg body weight) were supplemented daily with 0, 5, 10 or 20 mg lutein for 12 weeks. Delayed-type hypersensitivity (DTH) response to saline, phytohemagglutinin (PHA) and a polyvalent vaccine was assessed on Weeks 0, 6 and 12. Blood was sampled on Weeks 0, 2, 4, 8 and 12 to assess (1) lymphocyte proliferative response to PHA, concanavalin A (Con A), and pokeweed mitogen (PWM), (2) changes in peripheral blood mononuclear cell (PBMC) populations, (3) interleukin-2 (IL-2) production and (4) IgG and IgM production. After the completion of 12-week study, we continued to collect the blood weekly up to 17 weeks to evaluate the changes in immunoglobulin production upon first and second antigenic challenges on Weeks 13 and 15. Plasma lutein+zeaxanthin was undetectable in unsupplemented dogs but concentrations increased ( P<0.05) rapidly on Week 2 in lutein-supplemented dogs. Thereafter, concentrations generally continued to increase in dose-dependent manner, albeit at a much slower rate. Dogs fed lutein had heightened DTH response to PHA and vaccine by Week 6. Dietary lutein increased ( P<0.05) lymphocyte proliferative response to all three mitogens and increased the percentages of cells expressing CD5, CD4, CD8 and major histocompatibility complex class II (MHC II) molecules. The production of IgG increased ( P<0.05) in lutein-fed dogs after the second antigenic challenge. Lutein did not influence the expression of CD21 lymphocyte marker, plasma IgM or IL-2 production. Therefore, dietary lutein stimulated both cell-mediated and humoral immune responses in the domestic canine.

Modulation of humoral and cell-mediated immune responses by dietary lutein in cats

The immuno-modulatory role of dietary lutein in domestic cats is unknown. Female Tabby cats (10-month old; n=56) were supplemented daily for 12 weeks with 0, 1, 5 or 10 mg lutein. Blood was collected on Weeks 0, 2, 4, 8 and 12 to assess the following: (1) mitogen-induced peripheral blood mononuclear cells (PBMCs) proliferation, (2) changes in PBMC subpopulations, (3) interleukin-2 (IL-2) production and (4) plasma immunoglobulin (Ig)G production. In addition, delayed-type hypersensitivity (DTH) response to concanavalin A (Con A) or a polyvalent vaccine was performed on Weeks 0, 6 and 12. Dietary lutein increased plasma lutein concentrations in a dose-dependent manner ( p<0.001) and concentrations had not reached steady state after 12 weeks of feeding in cats given 5 or 10 mg lutein. Concentrations of plasma retinol and α-tocopherol were not influenced by diet. The DTH response to vaccine but not to Con A increased ( p<0.05) in a dose-dependent manner on Week 6. Compared to control, cats fed lutein also showed enhanced Con A- and pokeweed mitogen-stimulated PBMCs proliferation. Dietary lutein also increased the percentages of CD4+ and CD21+ lymphocytes on Week 12 but had no significant effect on pan T, CD8 and MHC class II markers. Plasma IgG was higher ( p<0.05) in cats fed 10 mg lutein on Weeks 8 and 12. These results support the immuno-modulatory action of lutein in domestic cats.

Dietary Lutein But Not Astaxanthin or β-Carotene Increases pim-1 Gene Expression in Murine Lymphocytes

This study investigates the effect of dietary carotenoids on pim-1 gene expression in mouse splenocytes. Female BALB/c mice were fed 0%, 0.02%, or 0.4% astaxanthin, β-carotene, and lutein for two weeks. Plasma and liver were obtained for the analysis of carotenoids. Splenocytes were isolated and cultured in the presence of concanavalin A, and the level of pim-1 mRNA was determined by Northern blot analysis. None of the carotenoids were detectable in the plasma and liver of unsupplemented mice. In plasma the concentration of astaxanthin (4.9-54.7 μmol/l) was dramatically higher than that of lutein (1.4-2.0 μmol/l) and β-carotene (0.1-0.7 μmol/l). Carotenoid uptake by the spleen but not the liver reflected that observed in plasma. In mice fed 0.4% of each carotenoid, the absolute concentration of the carotenoid in the liver was highest for astaxanthin (24 nmol/g) followed by b-carotene (7.5 nmol/g) and lutein (1.58 nmol/g). Mice fed lutein showed a dose-related increase in pim-1 mRNA expression. The steady-state level of pim-1 mRNA in mice fed 0.4% lutein was sixfold higher than in mice fed 0.02% lutein. In contrast, dietary astaxanthin and β-carotene did not affect pim-1 expression. Therefore, an increase in pim-1 mRNA was observed in splenocytes stimulated with concanavalin A in lutein-fed mice. This appears to be a unique effect of lutein and may be associated with its antitumor activity observed in vivo.

Dietary Lutein from Marigold Extract Inhibits Mammary Tumor Development in BALB/c Mice

High levels of dietary lutein can inhibit mammary tumor growth in mice. However, the antitumor effect of low levels of dietary lutein on mammary tumors is unavailable. Female BALB/c mice and the WAZ-2T (−SA) mammary tumor cell line were used in two experiments. A preliminary tumor cell dose titration study (Experiment 1) was designed to determine the inoculation dose to produce ∼65% tumor incidence. Mice (n = 10/dose) were inoculated with 0 to 1 × 106 tumor cells in the right inguinal mammary fat pad. A tumor cell load of 2.5 × 103 cells/inoculation produced ∼65% tumor incidence. This dose was used in a subsequent study (Experiment 2) of the efficacy of dietary lutein against mammary tumor development. Mice (n = 20/treatment) were fed a semisynthetic diet containing 0, 0.002, 0.02, 0.2 or 0.4% lutein from marigold extract. After 14 d, all mice were inoculated with 2.5 × 103 tumor cells, and tumor growth was measured daily for 70 d at which time blood, liver, spleen and tumors were obtained. Lutein + zeaxanthin uptake increased dose-dependently (P < 0.05) with dietary lutein levels from 0 to 0.02% (spleen) or 0.2% (plasma, liver and tumor). Low levels (0.002 and 0.02%) of dietary lutein lowered (P < 0.05) mammary tumor incidence, tumor growth and lipid peroxidation, and increased tumor latency, whereas higher dietary levels (0.2 or 0.4%) were less effective. Therefore, very low amounts of dietary lutein (0.002%) can efficiently decrease mammary tumor development and growth in mice.

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 μmol/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.

Isolation, structural elucidation, and partial synthesis of lutein dehydration products in extracts from human plasma

All- E-(3 R,6′ R)-3-hydroxy-3′,4′-didehydro- β, γ-carotene (anhydrolutein I) and all- E-(3 R,6′ R)-3-hydroxy-2′,3′-didehydro- β, ϵ-carotene (2′,3′-anhydrolutein II) have been isolated and characterized from extracts of human plasma using semipreparative high-performance liquid chromatography (HPLC) on a C 18 reversed-phase column. The identification of anhydroluteins was accomplished by comparison of the UV-Vis absorption and mass spectral data as well as HPLC-UV-Vis-mass spectrometry (MS) spiking experiments using fully characterized synthetic compounds. Partial synthesis of anhydroluteins from the reaction of lutein with 2% H 2SO 4 in acetone, in addition to anhydrolutein I (54%) and 2′,3′-anhydrolutein II (19%), also gave (3′ R)-3′-hydroxy-3,4-dehydro- β-carotene (3′,4′-anhydrolutein III, 19%). While anhydrolutein I has been shown to be usually accompanied by minute quantities of 2′,3′-anhydrolutein II (ca. 7–10%) in human plasma, 3′,4′-anhydrolutein III has not been detected. The presence of anhydrolutein I and II in human plasma is postulated to be due to acid catalyzed dehydration of the dietary lutein as it passes through the stomach. These anhydroluteins have also been prepared by conversion of lutein diacetate to the corresponding anhydrolutein acetates followed by alkaline hydrolysis. However, under identical acidic conditions, loss of acetic acid from lutein diacetate proceeded at a much slower rate than dehydration of lutein. The structures of the synthetic anhydroluteins, including their absolute configuration at C(3) and C(6′) have been unambiguously established by 1H NMR and in part by 13C NMR, and circular dichroism.

Effect of Coccidiosis on the Distribution of Dietary Lutein in the Chick

A series of experiments was run to determine whether the distribution of dietary carotenoids in chick plasma and tissue was dependent upon a saturable carrier, and to observe how infection with Eimeria acervulina affected this distribution. Broiler (Hubbard × Hubbard) and Sex Sal (Rhode Island Red × White Rock) chicks were fed a white corn and soybean meal-based diet supplemented with varying levels of a commercial lutein concentrate. Plasma, small intestine, and liver were analyzed for lutein. In the first experiment, mean plasma values in control broiler chicks increased linearly from 0 to 200 ppm supplementation. Mean plasma values of infected chicks were decreased an average of 71% as compared with controls, and reached a plateau between 100 and 200 ppm dietary lutein. In the second experiment, plasma, small intestinal, and liver lutein levels in broiler chicks reached a plateau between 200 and 500 ppm. In the third experiment, plasma and liver values in Sex Sal chicks leveled off between 250 and 500 ppm whereas levels in the small intestine increased linearly. Infection of the Sex Sal chicks at 3 wk of age with E. acervulina caused plasma lutein levels to be reduced about 88%, small intestinal levels 76%, and liver levels 72%. Supplementation with 500 ppm resulted in higher proportions of lutein in tissues. Infection with E. acervulina shifted the ratios to even higher proportions in the tissues at all supplementation levels. The results of the current study are consistent with the hypothesis that a carrier is required to mobilize lutein from tissues (particularly the intestinal mucosa) to the plasma, and further, that E. acervulina infection adversely affects levels of this carrier.

Antioxidant activity of xanthophylls on peroxyl radical-mediated phospholipid peroxidation

The ability of xanthophylls (canthaxanthin, zeaxanthin, and astaxanthin) as chain-breaking antioxidants was investigated in peroxyl radical-mediated peroxidation of phosphatidylcholine (PC) liposomes under atmospheric conditions using lipid-soluble and water-soluble radical generators. These xanthophylls retarded the chain propagation reaction of phosphatidylcholine hydroperoxides (PC-OOH) formation, although their activities to trap chain-carrying peroxyl radical were much less than that of alpha-tocopherol. In chick plasma studies, it was observed that endogenious xanthophylls participated in the antioxidant defenses against the attack of aqueous peroxyl radical. It was concluded that xanthophylls possess the ability to act as chain-breaking antioxidants in the peroxidation of membraneous phospholipids. Dietary xanthophylls may, therefore, be helpful in resisting membraneous phospholipids against oxidative damage in vivo.

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 μg lutein/g diet and with varying amounts of aflatoxin (0, 1, 2, 4, and 8 μg/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.

3′-Oxolutein, a Metabolite of Lutein in Chickens ,

3′-Oxolutein (3-hydroxy-3′-oxo-β,ε-carotene) was isolated using high performance liquid chromatography (HPLC) from the tissues and egg yolks of chickens fed a diet high in lutein and free of detectable 3′-oxolutein. It was identified by HPLC retention time, absorption spectrum identical to lutein and its esters, disappearance under alkaline conditions without giving rise to lutein, formation of an alkali labile palmitate, formation of a 2,4-dinitrophenylhydrazone, and reduction to lutein from which the dipalmitate was prepared. In each instance the isolated compound behaved identically with authentic 3′-oxolutein prepared by nickel peroxide oxidation of lutein. The order of ratios of lutein to 3′-oxolutein in the various tissues from laboratory and field birds was, in general, intestinal contents > intestinal mucosa > serum > liver ~ toe web ~ egg yolk > bile. This order was consistent with the hypothesis that lutein was oxidized to 3′-oxolutein in the liver, which, at least in part, was excreted via the bile into the intestinal lumen where it was diluted with dietary lutein. The remainder of the 3′-oxolutein formed in the liver presumably went into the serum where it was transported to depot sites. The ratio of lutein to 3′-oxolutein in the toe webs of broilers varied with their diet and pigmentation status. Amounts of 3′-oxolutein were found in quail and turkey egg yolks. This previously unreported lutein oxidative capability of liver extends the previously known metabolic acylation and deacylation reactions in poultry.

The Effect of Saponification on the Broiler Coloring Capability of Marigold Extracts

Two experiments were conducted to compare the broiler skin coloring capabilities of a saponified and nonsaponified marigold concentrate. In both experiments, 260 male broiler chicks, 1 day of age, were randomly assigned to eight pens, each pen receiving one of two test diets formulated to contain the same total xanthophyll from either a saponified or nonsaponified marigold extract. In Experiment 1, a white corn basal diet was utilized so that dietary xanthophyll was entirely supplied by the test products. In Experiment 2, the diets were formulated identically to Experiment 1, except that yellow corn was substituted for white corn, and the added xanthophyll from the marigold products reduced accordingly. The broilers were processed at 49 days of age. Carcass skin and shank color were evaluated by reflectance colorimetry. Shank color was also evaluated by visual scoring with the Roche Color Fan (RCF). Saponification of the marigold concentrate resulted in significantly (P<.05 ) increased skin yellowness (b*) values of 38.8 and 37.4, as measured by reflectance colorimetry, relative to those values produced by the nonsaponified marigold product, 24.9 and 29.7, in Experiments 1 and 2, respectively. In the same respective comparison, shank yellowness (b*) values for the saponified samples were 68.7 and 70.1, significantly (P<.05) greater relative to the nonsaponified sample values of 55.3 and 63.8 in both experiments. Shank color, as measured by the RCF were also significantly (P<.05) greater for saponified samples, 8.0 and 7.1, compared to the nonsaponified values of 4.4 and 5.3 in Experiments 1 and 2, respectively. The results suggested that the saponification of marigold extracts will produce highly significant increases in the broiler coloring capability of such products. The increased capability was more apparent when the white corn basal diet was used.