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PubMed2002

Interictal and postictal alterations of pulsatile secretions of luteinizing hormone in temporal lobe epilepsy in men.

Mesial temporal lobe epilepsy has been associated with abnormalities of reproductive physiology, but the mechanisms of hormonal dysregulation are not clear. Chronic effects of the epileptic state and the acute impact of seizures could alter hypothalamic function, which is represented by the downstream pulsatile secretion of luteinizing hormone. This study evaluates the interictal and postictal secretion of luteinizing hormone in mesial temporal lobe epilepsy. We characterized luteinizing hormone secretion in patients with mesial temporal lobe epilepsy during two 24-hour epochs: an interictal baseline and a postictal interval initiated by an electrographically confirmed spontaneous seizure. Males, rather than females, were studied so that menstrual cycles could not account for differences between epochs. Blood luteinizing hormone and prolactin (as a positive control) were measured every 10 minutes. Deconvolution analysis defined luteinizing hormone secretion in terms of interpulse interval, amplitude, and mass. Approximate entropy quantitated relative degradation in the orderliness of serial luteinizing hormone release. Interictal baseline epochs were compared to those of healthy controls with unpaired Student's t tests and between interictal and postictal epochs within epileptic patients with paired t tests. Ten epileptic men completed both interictal and postictal epochs. Interictally, seizure patients had lower mean concentrations, slower pulse rates, and higher peak amplitudes than healthy male controls. Within epileptic patients, mean interpulse interval, pulse amplitude, and pulse mass were not affected by the occurrence of seizures, whereas the orderliness of pulse mass decreased postictally. Acute seizures induced timing irregularity in luteinizing hormone secretion, whereas chronic epilepsy was associated with changes in luteinizing hormone pulse frequency, amplitude, and mass. Altered timing and regularity of neuroendocrine pulse patterns may underlie other disorders of homeostasis in mesial temporal lobe epilepsy.

Adult↗
PubMed2005

Low doses of beta-carotene and lutein inhibit AOM-induced rat colonic ACF formation but high doses augment ACF incidence.

Epidemiological studies suggest that carotenoids such as beta-carotene and lutein play an important role in reducing the risk for several cancers. However, in colon cancer there is ambiguity with regard to the role of these compounds in that both preventive effects and tumor promotion have been observed. In the present study we observed that male F344 rats were able to tolerate up to 2,500 ppm of beta-carotene as well as of lutein. We have then assessed the chemopreventive efficacy of beta-carotene and lutein at dose levels of approximately 4 and 8% of the 2,500 ppm tolerated dose (TD) and also approximately 40 and 80% of the TD on azoxymethane (AOM)-induced colon carcinogenesis, using aberrant crypt foci (ACF) as a surrogate biomarker for colon cancer. Throughout the experiments, 5-week-old male F344 rats were fed the control diet (modified AIN-76A) or experimental diets containing 100 or 200 ppm (approximately 4 or 8% of the 2,500 ppm TD), or 1,000 or 2,000 ppm ( approximately 40 or 80% of the 2,500 ppm TD) of beta-carotene and lutein (n=10 rats/group). After 2 weeks on the experimental or control diets, all animals were injected with AOM (15 mg/kg body wt., once weekly for 2 weeks). At 14 weeks of age, all rats were killed, and their colons were evaluated for ACF. Administration of 100 or 200 ppm of beta-carotene inhibited AOM-induced total colonic ACF formation by 24% (p<0.01) and 36% (p<0.001), respectively, whereas lutein at 200 ppm produced a 27% inhibition (p<0.01) yet had no significant effect at the 100 ppm dose level. Surprisingly, administration of 1,000 or 2,000 ppm of beta-carotene and lutein increased colonic ACF formation in a dose-dependent manner, i.e., to 124% and 144% for the former and 110% and 159% for the latter. These results clearly suggest that further studies are warranted to determine whether the increase in ACF incidence by high doses of beta-carotene and lutein will also lead to an increase in tumor outcome. Taken together these data indicate that the chemopreventive activity of beta-carotene and lutein against colon carcinogenesis depends on the dose level.

Animals↗
PubMed1994

Modulation by cortisol of luteinizing hormone secretion from cultured porcine anterior pituitary cells: effects on secretion induced by phospholipase C, phorbol ester and cAMP.

Cultures of enzymatically dispersed porcine anterior pituitary cells were used to examine the effects of cortisol on luteinizing hormone secretion induced by a variety of compounds which activate different intracellular signal transduction mechanisms. Cells were pre-incubated with or without cortisol (200 micrograms/ml) for 3 days, washed and then incubated for 4 h with or without cortisol in the presence or absence of these compounds. Luteinizing hormone in the media was assayed by radioimmunoassay. Cortisol treatment had no effect on basal luteinizing hormone release, but reduced gonadotropin-releasing hormone (8.5 x 10(-8) mol/l) stimulated luteinizing hormone secretion. Phospholipase C, 8-bromo-cyclic adenosine 3',5'-monophosphate, and 12-O-tetradecanoyl-phorbol-13-acetate (an activator of protein kinase C) all stimulated luteinizing hormone secretion in a dose-dependent manner in cortisol-untreated cells. Pretreatment with cortisol inhibited luteinizing hormone secretion induced by phospholipase C and 8-bromo-cyclic adenosine 3',5'-monophosphate, but did not affect the secretion of luteinizing hormone in response to 12-O-tetradecanoyl-phorbol-13 acetate. Cortisol inhibited GnRH-induced inositol phosphate production. Our results suggest that the inhibitory action of cortisol on stimulus-coupled luteinizing hormone secretion may be exerted at two different intracellular sites: (1) by inhibition of phospholipase C activity and (2) at a point distal to cyclic adenosine 3',5'-monophosphate generation.

Animals↗
PubMed1995

Gonadotropin-releasing hormone antagonist versus agonist administration in women undergoing controlled ovarian hyperstimulation: cycle performance and in vitro steroidogenesis of granulosa-lutein cells.

OBJECTIVES: We sought to determine the effectiveness of a gonadotropin-releasing hormone antagonist compared with an agonist in suppressing a spontaneous luteinizing hormone surge in women undergoing controlled ovarian hyperstimulation for in vitro fertilization and gamete intrafallopian transfer and to examine whether in vivo administration of these analogs effects granulosa-lutein cells steroidogenesis in vitro. STUDY DESIGN: This prospective case-control study included 30 healthy women undergoing ovarian hyperstimulation with human menopausal gonadotropins. Fifteen women received the Nal-Glu antagonist, 5 mg intramuscularly daily, when the lead follicle was > or = 15 mm or serum estradiol level was > or = 500 pg/ml. The control group included 15 women who underwent oocyte retrieval on the same day as the study subjects and were given the agonist leuprolide acetate, 250 micrograms subcutaneously daily, starting on cycle day 1. Granulosa-lutein cells were purified from follicular aspirates from six subjects and six controls and cultured in parallel, evaluating basal progesterone production, progesterone response to follicle-stimulating hormone or luteinizing hormone and aromatase activity. RESULTS: No difference was demonstrated in the total amount of gonadotropins received by the two groups. Overall, the gonadotropin-releasing hormone antagonist was given for only 2.5 +/- 0.2 (mean +/- SEM) days before human chorionic gonadotropin administration. The antagonist group showed significantly lower levels of serum luteinizing hormone than did the agonist group, 1.0 +/- 0.2 versus 4.2 +/- 0.5 mIU/ml (p = 0.0001) on the day of human chorionic gonadotropin administration. Serum estradiol levels were significantly lower in the antagonist than the agonist group, 820 +/- 120 versus 1361 +/- 110 pg/ml (p = 0.003) on the day of human chorionic gonadotropin administration. There was no difference in the number of retrieved oocytes, but the antagonist group had a higher proportion of mature oocytes, 82% +/- 4% versus 62.4% (p = 0.02), and a higher proportion of embryos of good quality, 69.8% +/- 9.8% versus 44.3% +/- 7.2% (p = 0.03) in the agonist group. Granulosa-lutein cells from antagonist-treated women showed significantly lower aromatase activity the first 6 hours after retrieval, 17.6 +/- 1.6 versus 31.3 +/- 7.4 ng/ml per 6 hours estradiol (p = 0.03), whereas basal and gonadotropin-stimulated with progesterone responses were similar. CONCLUSION: Gonadotropin-releasing hormone antagonist administration during the late follicular phase resulted in lower serum luteinizing hormone and estradiol levels and more mature oocytes and embryos of better quality compared with gonadotropin-releasing hormone agonist administration. These results suggest that gonadotropin-releasing hormone antagonist administration in ovarian hyperstimulation has practical advantages over the agonist regimen. Gonadotropin-releasing hormone analogs may have direct action on ovarian function with differential effects on granulosa-lutein cell aromatase activity. This could explain the lower serum estradiol levels routinely observed in women given gonadotropin-releasing hormone antagonist.

Adult↗
PubMed2005

Photooxidation of A2-PE, a photoreceptor outer segment fluorophore, and protection by lutein and zeaxanthin.

A2-PE is a pigment that forms as a byproduct of the visual cycle, its synthesis from all-trans-retinal and phosphatidylethanolamine occurring in photoreceptor outer segments. A2-PE is deposited in retinal pigment epithelial (RPE) cells secondary to phagocytosis of shed outer segment membrane and it undergoes hydrolysis to generate the RPE lipofuscin fluorophores, A2E, iso-A2E and other minor cis-isomers of A2E. We have demonstrated that A2-PE can initiate photochemical processes that involve the oxidation of A2-PE and that, by analogy with A2E are likely to include the formation of reactive moieties. We also show that potential sources of protection against the photooxidation of A2-PE are the lipid-soluble carotenoids zeaxanthin and lutein (xanthophylls), that constitute the yellow pigment of the macula. Irradiation of A2-PE in the presence of lutein or zeaxanthin suppressed A2-PE photooxidation and in experiments in which we compared the antioxidant capability of zeaxanthin and lutein to alpha-tocopherol, the carotenoids were more potent. Additionally, the effect with zeaxanthin was consistently more robust than with lutein and when alpha-tocopherol was combined with either carotenoid, the outcome was additive. Lutein, zeaxanthin and alpha-tocopherol were all efficient quenchers of singlet oxygen. We have also shown that lutein and zeaxanthin can protect against A2-PE/A2E photooxidation without appreciable consumption of the carotenoid by chemical reaction. This observation contrasts with the pronounced susceptibility of A2E and A2-PE to photooxidation and is of interest since lutein, zeaxanthin, A2E and A2-PE all have conjugated systems of carbon-carbon double bonds terminating in cyclohexenyl end-groups. The structural features responsible for the differences in quenching mechanisms are discussed. It has long been suspected that macular pigment protects the retina both by filtering high-energy blue light and by serving an antioxidant function. Evidence presented here suggests that the photochemical reactions against which lutein and zeaxanthin protect, may include those initiated by the A2-PE. Quantitative HPLC analysis revealed that in eyecups of C57BL/6J and BALB/cByJ mice, levels of A2-PE were several fold greater than the cleavage product, A2E. Taken together, these results may have implications with respect to the involvement of A2-PE formation in mechanisms underlying blue light-induced photoreceptor cell damage and may be significant to retinal degenerative disorders, such as those associated with ABCA4 mutations, wherein there is a propensity for increased A2-PE synthesis.

Animals↗
PubMed2005

Ultrasound assisted extraction in quantifying lutein from chicken liver using high-performance liquid chromatography.

Four sample preparation methods, (1) solvent (SOL), (2) saponification and solvent (SP), (3) ultrasound assisted solvent (UA), and (4) saponification and ultrasound assisted solvent (SP-UA), were used for quantifying lutein in chicken liver samples by HPLC. The lutein concentrations obtained by using SOL, UA, SP, and SP-UA were significantly different with values from 10.4 microg/g (UA) to undetected (SOL). Efficiency of the four different methods for extracting lutein from high to low were the UA, SP, SP-UA, and SOL method. The measured value of lutein in the liver sample using the UA method was approximately two and three times higher than that obtained from the SP and SP-UA method, respectively. The methods with saponification significantly affected the stabilities of lutein in liver samples. The lutein concentration measured with the solvent only method was either much lower than any of the other extraction methods or undetectable. This indicated that little lutein in those samples was in a form that could be extracted directly by solvent. Compared with the saponification method, the ultrasound assisted solvent method could effectively extract lutein from sample matrix and thus avoid chemical degradation reactions, which would be especially important for complex biological tissue such as liver.

Animals↗
PubMed2000

Organisation of xanthophyll pigments lutein and zeaxanthin in lipid membranes formed with dipalmitoylphosphatidylcholine.

Carotenoid pigments and in particular xanthophylls play several physiological functions in plant and animal membranes. Xanthophylls are present in biological membranes in the form of pigment-protein complexes but also as direct components of lipid phase. The biological activity of carotenoids in membranes depends on a molecular organisation of pigments in lipid bilayers, in particular the localisation, orientation and aggregational state. In the present work the organisation of lutein- and zeaxanthin-containing lipid membranes was analysed with the application of electronic absorption spectroscopy. Both xanthophyll pigments incorporated to the dipalmitoylphosphatidylcholine (DPPC) unilamellar liposomes form H-type molecular aggregates, manifested by the hypsochromic shift of the main absorption band of carotenoids. The aggregation of lutein and zeaxanthin in DPPC membranes was observed even at relatively low concentrations of a pigment in the lipid phase (1-5 mol%). Gaussian analysis of the absorption spectra of lutein and zeaxanthin in DPPC membranes in terms of the exciton splitting theory revealed the formation of different molecular structures of pigments interpreted as dimers, trimers, tetramers and large aggregates. The fraction of lutein and zeaxanthin in the monomeric form was found to depend on the physical state of the lipid phase. Pronounced monomerisation of lutein and zeaxanthin was observed as accompanying the transition from the P(beta)' phase to the L(alpha) phase of DPPC, mostly at the expense of the trimeric and tetrameric forms. The fraction of monomers of lutein is always lower by 10-30% than that of zeaxanthin under the same experimental conditions. Different organisational forms of lutein and zeaxanthin in the model system studied are discussed in terms of possible physiological functions of these pigments in the membranes of the retina: zeaxanthin in the protection of the lipid phase against oxidative damage and lutein in absorbing short wavelength radiation penetrating retina membranes.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2000

Carotenoid content of chlorophycean microalgae: factors determining lutein accumulation in Muriellopsis sp. (Chlorophyta).

Fifteen strains of chlorophycean microalgae have been investigated with regard to their carotenoid profile. Lutein, beta-carotene and violaxanthin were present in virtually all of the strains, lutein, in general, being the most abundant carotenoid, whereas canthaxanthin and astaxanthin were found in some strains only. Chlorella fusca SAG 211-8b, Chlorococcum citriforme SAG 62.80, Muriellopsis sp., Neospongiococcum gelatinosum SAG B 64.80 and Chlorella zofingiensis CCAP 211/14 exhibited high lutein levels, the latter strain containing in addition substantial amounts of astaxanthin. Muriellopsis sp. was further characterized, since besides a high lutein content (up to 35 mg l(-1) culture), it had the highest growth rate (up to 0.17-0.23 h(-1)) and maximal standing cell density (up to 8 x 10(10) cells l(-1) culture). These levels of lutein are in the range of those reported for astaxanthin in Haematococcus and for beta-carotene in Dunaliella, microalgae of recognized interest for the production of these carotenoids. Lutein content of Muriellopsis sp. increased during the exponential phase of growth, with the highest value being recorded in the early stationary phase. Maximum levels of lutein in Muriellopsis sp. cultures were recorded at 20-40 mM NaNO3, 2-100 mM NaCl, 460 micromol photon m(-2) s(-1), pH 6.5 and 28 degrees C, conditions which were, in general, also optimal for cell growth. Growth-limiting conditions, such as pH values of 6 or 9 and a temperature of 33 degrees C, were found to stimulate carotenogenesis in Muriellopsis sp. This strain represents a potential source of lutein, a commercially interesting carotenoid of application in aquaculture and poultry farming, as well as in the prevention of cancer and diseases related to retinal degeneration.

Cell Division↗
PubMed2003

Lutein, but not alpha-tocopherol, supplementation improves visual function in patients with age-related cataracts: a 2-y double-blind, placebo-controlled pilot study.

OBJECTIVE: We investigated the effect of long-term antioxidant supplementation (lutein and alpha-tocopherol) on serum levels and visual performance in patients with cataracts. METHODS: Seventeen patients clinically diagnosed with age-related cataracts were randomized in a double-blind study involving dietary supplementation with lutein (15 mg; n = 5), alpha-tocopherol (100 mg; n = 6), or placebo (n = 6), three times a week for up to 2 y. Serum carotenoid and tocopherol concentrations were determined with quality-controlled high-performance liquid chromatography, and visual performance (visual acuity and glare sensitivity) and biochemical and hematologic indexes were monitored every 3 mo throughout the study. Changes in these parameters were assessed by General Linear Model (GLM) repeated measures analysis. RESULTS: Serum concentrations of lutein and alpha-tocopherol increased with supplementation, although statistical significance was reached only in the lutein group. Visual performance (visual acuity and glare sensitivity) improved in the lutein group, whereas there was a trend toward the maintenance of and decrease in visual acuity with alpha-tocopherol and placebo supplementation, respectively. No significant side effects or changes in biochemical or hematologic profiles were observed in any of the subjects during the study. CONCLUSIONS: Visual function in patients with age-related cataracts who received the lutein supplements improved, suggesting that a higher intake of lutein, through lutein-rich fruit and vegetables or supplements, may have beneficial effects on the visual performance of people with age-related cataracts.

Age Factors↗
PubMedDate not supplied

High-yield production of lutein by the green microalga Chlorella protothecoides in heterotrophic fed-batch culture.

The green microalga Chlorella protothecoides was grown heterotrophically in batch mode in a 3.7-L fermenter containing 40 g/L glucose and 3.6 g/L urea. In the late exponential phase, concentrated nutrients containing glucose and urea were fed into the culture, in which the nitrogen source was sufficient compared to carbon source. As a result, a maximum cell dry weight concentration of 48 g/L was achieved. This cell dry weight concentration was 28.4 g/L higher than that obtained in batch culture under the same growth conditions. In another cultivation run, the culture was provided with the same initial concentrations of glucose (40 g/L) and urea (3.6 g/L) as in the batch mode, followed by a relatively reduced supply of nitrogen source in the fed-batch mode to establish a nitrogen-limited culture. Such a modification resulted in an enhanced lutein production without significantly lowering biomass production. The cellular lutein content was 0.27 mg/g higher than that obtained in the N-sufficient culture. The improvements were also reflected by higher maximum lutein yield, lutein productivity, and lutein yield coefficient on glucose. This N-limited fed-batch culture was successfully scaled up from 3.7 L to 30 L, and a three-step cultivation process was developed for the high-yield production of lutein. The maximum cell dry weight concentration (45.8 g/L) achieved in the large fermenter (30 L) was comparable to that in the small one (3.7 L). The maintenance of the culture at a higher temperature (i.e., 32 degrees C) for 84 h resulted in a 19.9% increase in lutein content but a 13.6% decrease in cell dry weight concentration as compared to the fed-batch culture (30 L) without such a treatment. The enhancement of lutein production resulted from the combination of nitrogen limitation and high-temperature stress.

Biomass↗
PubMed2003

Distribution of lutein, zeaxanthin, and related geometrical isomers in fruit, vegetables, wheat, and pasta products.

Quantitative data with regard to dietary (3R,3'R,6'R)-lutein, (3R,3'R)-zeaxanthin, and their (E/Z)-geometrical isomers are scarce, and in most cases, only the combined concentrations of these two carotenoids in foods are reported. Lutein and zeaxanthin accumulate in the human macula and have been implicated in the prevention of age-related macular degeneration (AMD). The qualitative and quantitative distributions of lutein, zeaxanthin, and their (E/Z)-isomers in the extracts from some of the most commonly consumed fruits, vegetables, and pasta products were determined by HPLC employing a silica-based nitrile-bonded column. Green vegetables had the highest concentration of lutein (L) and zeaxanthin (Z), and the ratios of these carotenoids (L/Z) were in the range 12-63. The yellow-orange fruits and vegetables, with the exception of squash (butternut variety), had much lower levels of lutein in comparison to greens but contained a higher concentration of zeaxanthin. The ratio of lutein to zeaxanthin (L/Z) in two North American bread varieties of wheat (Pioneer, Catoctin) was 11 and 7.6, respectively, while in a green-harvested wheat (Freekeh) imported from Australia, the ratio was 2.5. Between the two pasta products examined, lasagne and egg noodles, the latter had a much higher concentration of lutein and zeaxanthin. The levels of the (E/Z)-geometrical isomers of lutein and zeaxanthin in these foods were also determined.

Chromatography, High Pressure Liquid↗
PubMed1969

Glucose metabolism in the superovulated rat ovary in vitro. Effects of luteinizing hormone and the role of glucose metabolism in steroidogenesis.

1. Superovulated rat ovary slices from rats treated with 20mug. of luteininzing hormone/100g. body wt. 2hr. before death and from control animals have been incubated in vitro. Output of Delta(4)-3-oxo steroids (0.2mumole/g. wet wt./hr. in control tissue) was linear for 4hr., and was increased by approx. 70% in slices from luteinizing hormone-treated rats. Rate of oxygen consumption (90.0+/-4.6mumoles/g. wet wt./hr.) was linear for 3hr. and unaltered by luteinizing hormone treatment or addition of glucose (1mg./ml.) to the medium. 2. In slices from control animals, steady-state rate of glucose uptake was 78.0+/-2.9mug. atoms of carbon/g. wet wt./hr.; steady-state rates of lactate output, pyruvate output and incorporation of [U-(14)C]-glucose carbon atoms into carbon dioxide and total lipid extract were 60.7+/-0.9, 2.4+/-0.1, 18.0+/-1.1 and 0.7+/-0.1mug. atom of carbon/g. wet wt./hr. and accounted for 104.5+/-1.9% of the glucose uptake. In slices from luteinizing hormone-treated rats, glucose uptake and outputs of lactate, pyruvate and [(14)C]carbon dioxide were increased by approx. 25%, and 108.4+/-3.2% of the glucose uptake could be accounted for. 3. The total lipid extract was separated by thin-layer chromatography and saponification. Of the (14)C incorporated into this fraction during incubation with [U-(14)C]glucose 97% was found in the fractions containing glyceride glycerol and less than 3% in the fractions containing sterols, steroids or fatty acids. Appreciable quantities of (14)C were incorporated into these lipid fractions from [1-(14)C]acetate. 4. From a consideration of the tissue glycogen content, the specific activities of [(14)C]lactate and glucose 6-phosphate (C-1) derived from [1-(14)C]-, [6-(14)C]- and [U-(14)C]-glucose, and the ratio of [(14)C]carbon dioxide yields from [1-(14)C]glucose and [6-(14)C]glucose, it was concluded that there was no appreciable glycogenolysis or flow through the pentose phosphate cycle. 5. In ovary slices from both control and luteinizing hormone-treated animals, glucose in vitro raised the incorporation rate of (14)C from [1-(14)C]acetate into sterols and steroids. Luteinizing hormone in vivo stimulated the incorporation rate in vitro but only in the presence of glucose. 6. In slices incubated in medium containing [(3)H]water, [(14)C]sorbitol and glucose (1mg./ml.), the total water space (865+/-7.1mul./g.) and the extracellular water space (581+/-22mul./g.) were unchanged by luteinizing hormone treatment in vivo but the glucose space was raised from 540+/-23.6mul./g. to 639+/-31.3mul./g. 7. Luteinizing hormone treatment was found to lower the tissue concentration of the hexose monophosphates and to increase the total activity of hexokinase, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase and possibly of phosphofructokinase. 8. The kinetic properties of a partially purified preparation of phosphofructokinase were found to be qualitatively similar to those from other mammalian tissues. 9. The results are discussed with reference to both the role of glucose metabolism in steroidogenesis and the mechanism by which luteinizing hormone increases the rate of glucose uptake.

Acetates↗
PubMed1996

Purification and partial characterization of a lutein-binding protein from the midgut of the silkworm Bombyx mori.

A lutein-binding protein was purified from fifth instar larval midgut of Bombyx mori by a combination of ammonium sulfate fractionation and three chromatographic procedures, gel filtration, chromatofocusing, and anion exchange chromatography. The protein has a pI of 5.4 and an apparent molecular mass of 35,000 Da, as determined by a linear gradient SDS-polyacrylamide gel electrophoresis. The lutein-protein complex is water-soluble and more stable than the carotenoid or protein alone. The carotenoid moiety was identified by thin layer chromatography, light absorption spectroscopy, and high performance liquid chromatography as all-trans-lutein. Lutein is specifically and stoichiometrically bound to the protein, with a ratio of 3 mol of lutein per mol of protein. Binding of lutein (absorption maximum in hexane at 454 nm) to the apoprotein results in a marked red spectral shift of about 38 nm, giving rise to absorption maxima at 432, 462, and 492 nm in 20 mM Tris-HCl, pH 7.0. The lutein-protein complex is characterized by fine spectral structure indicating that lutein is in a relatively rigid environment. This protein is distributed in equal amounts throughout the midgut and in all developmental stages of the larval B. mori.

Ammonium Sulfate↗
PubMed2003

Nutritional and clinical relevance of lutein in human health.

Lutein is one of the most widely found carotenoids distributed in fruits and vegetables frequently consumed. Its presence in human tissues is entirely of dietary origin. Distribution of lutein among tissues is similar to other carotenoids but, along with zeaxanthin, they are found selectively at the centre of the retina, being usually referred to as macular pigments. Lutein has no provitamin A activity in man but it displays biological activities that have attracted great attention in relation to human health. Epidemiological studies have shown inconsistent associations between high intake or serum levels of lutein and lower risk for developing cardiovascular disease, several types of cancer, cataracts and age-related maculopathy. Also, lutein supplementation has provided both null and positive results on different biomarkers of oxidative stress although it is effective in increasing macular pigment concentration and in improving visual function in some, but not all, subjects with different eye pathologies. Overall, data suggest that whereas serum levels of lutein have, at present, no predictive, diagnostic or prognostic value in clinical practice, its determination may be very helpful in assessing compliance and efficacy of intervention as well as potential toxicity. In addition, available evidence suggests that a serum lutein concentration between 0.6 and 1.05 micromol/l seems to be a safe, dietary achievable and desirable target potentially associated with beneficial impact on visual function and, possibly, on the development of other chronic diseases. The use of lutein as a biomarker of exposure in clinical practice may provide some rationale for assessing its relationship with human health as well as its potential use within the context of evidence-based medicine.

Biological Availability↗
PubMed2001

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

BACKGROUND: 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. OBJECTIVE: This study was designed to evaluate the relation between dietary intake, blood concentrations, and retinal concentrations of carotenoids in a large group of volunteers. DESIGN: 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. RESULTS: 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). CONCLUSIONS: 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.

Adult↗
PubMed1998

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 approximately 65% tumor incidence. Mice (n = 10/dose) were inoculated with 0 to 1 x 10(6) tumor cells in the right inguinal mammary fat pad. A tumor cell load of 2.5 x 10(3) cells/inoculation produced approximately 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 x 10(3) 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.

Animals↗
PubMed2006

Lutein is needed for efficient chlorophyll triplet quenching in the major LHCII antenna complex of higher plants and effective photoprotection in vivo under strong light.

BACKGROUND: Lutein is the most abundant xanthophyll in the photosynthetic apparatus of higher plants. It binds to site L1 of all Lhc proteins, whose occupancy is indispensable for protein folding and quenching chlorophyll triplets. Thus, the lack of a visible phenotype in mutants lacking lutein has been surprising. RESULTS: We have re-assessed the lut2.1 phenotypes through biochemical and spectroscopic methods. Lhc proteins from the lut2.1 mutant compensate the lack of lutein by binding violaxanthin in sites L1 and L2. This substitution reduces the capacity for regulatory mechanisms such as NPQ, reduces antenna size, induces the compensatory synthesis of Antheraxanthin + Zeaxanthin, and prevents the trimerization of LHCII complexes. In vitro reconstitution shows that the lack of lutein per se is sufficient to prevent trimerization. lut2.1 showed a reduced capacity for state I-state II transitions, a selective degradation of Lhcb1 and 2, and a higher level of photodamage in high light and/or low temperature, suggesting that violaxanthin cannot fully restore chlorophyll triplet quenching. In vitro photobleaching experiments and time-resolved spectroscopy of carotenoid triplet formation confirmed this hypothesis. The npq1lut2.1 double mutant, lacking both zeaxanthin and lutein, is highly susceptible to light stress. CONCLUSION: Lutein has the specific property of quenching harmful 3Chl* by binding at site L1 of the major LHCII complex and of other Lhc proteins of plants, thus preventing ROS formation. Substitution of lutein by violaxanthin decreases the efficiency of 3Chl* quenching and causes higher ROS yield. The phenotype of lut2.1 mutant in low light is weak only because rescuing mechanisms of photoprotection, namely zeaxanthin synthesis, compensate for the ROS production. We conclude that zeaxanthin is effective in photoprotection of plants lacking lutein due to the multiple effects of zeaxanthin in photoprotection, including ROS scavenging and direct quenching of Chl fluorescence by binding to the L2 allosteric site of Lhc proteins.

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PubMed1999

Dietary lutein but not astaxanthin or beta-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, beta-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 mumol/l) was dramatically higher than that of lutein (1.4-2.0 mumol/l) and beta-carotene (0.1-0.7 mumol/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 beta-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 beta-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.

Animals↗