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PubMed2004

Lutein supplements are not bioavailable in the Mongolian gerbil while consuming a diet with or without cranberries.

Lutein is a carotenoid that may be involved in the prevention of macular degeneration and is available as supplements. Cranberries are a potential "functional food" due to anti-adhesion and antioxidant properties. This study was designed to determine the bioavailability of lutein supplements in Mongolian gerbils, as prior studies have focused on beta-carotene, and to investigate any interactions between a lutein supplement and a diet containing cranberries. Gerbils (n = 28) were divided into treatment groups: lutein + cranberry; lutein + control; cottonseed oil + cranberry; and cottonseed oil + control. The lutein supplement (50 microg lutein in oil) was delivered orally for 14 days, and then blood, livers, and eyes were collected. Samples were analyzed by high-performance liquid chromatography (HPLC) and total antioxidant status was determined. Serum and liver were analyzed for lutein, retinol, and alpha-tocopherol. Serum lutein concentrations were extremely low in all four groups. Serum total antioxidants did not differ (p > 0.2) among diet groups. Serum retinol concentrations were significantly lower in the cranberry groups (p = 0.0024). In conclusion, gerbils are able to thrive on a high cranberry diet. However, this study showed that lutein, as a daily supplement in oil, is not bioavailable in Mongolian gerbils.

Animals↗
PubMed1996

Arabidopsis carotenoid mutants demonstrate that lutein is not essential for photosynthesis in higher plants.

Lutein, a dihydroxy beta, epsilon-carotenoid, is the predominant carotenoid in photosynthetic plant tissue and plays a critical role in light-harvesting complex assembly and function. To further understand lutein synthesis and function, we isolated four lutein-deficient mutants of Arabidopsis that define two loci, lut1 and lut2 (for lutein deficient). These loci are required for lutein biosynthesis but not for the biosynthesis of beta, beta-carotenoids. The lut1 mutations are recessive, accumulate high levels of zeinoxanthin, which is the immediate precursor of lutein, and define lut1 as a disruption in epsilon ring hydroxylation. The lut2 mutations are semidominant, and their biochemical phenotype is consistent with a disruption of epsilon ring cyclization. The lut2 locus cosegregates with the recently isolated epsilon cyclase gene, thus, providing additional evidence that the lut2 alleles are mutations in the epsilon cyclase gene. It appears likely that the epsilon cyclase is a key step in regulating lutein levels and the ratio of lutein to beta,beta-carotenoids. Surprisingly, despite the absence of lutein, neither the lut1 nor lut2 mutation causes a visible deleterious phenotype or altered chlorophyll content, but both mutants have significantly higher levels of beta, beta-carotenoids. In particular, there is a stable increase in the xanthophyll cycle pigments (violaxanthin, antheraxanthin, and zeaxanthin) in both lut1 and lut2 mutants as well as an increase in zeinoxanthin in lut1 and beta-carotene in lut2. The accumulation of specific carotenoids is discussed as it pertains to the regulation of carotenoid biosynthesis and incorporation into the photosynthetic apparatus. Presumably, particular beta, beta-carotenoids are able to compensate functionally and structurally for lutein in the photosystems of Arabidopsis.

Arabidopsis↗
PubMed2006

Inhibitory effects of lutein on endotoxin-induced uveitis in Lewis rats.

PURPOSE: Lutein deposits in the macula and lens of human eyes with high concentration and is well known as an eye-protective nutrient for its beneficial effects on eye disease such as age-related macular degeneration and cataract. The purpose of the present study was to investigate the effects of lutein on endotoxin-induced uveitis (EIU) in rats. METHODS: EIU was induced in male Lewis rats by subcutaneous injection of 200 microg lipopolysaccharide. Lutein or dexamethasone was administered intravenously at 30 minutes before, at the same time as, and at 30 minutes after LPS treatment. The aqueous humor was collected at 24 hours after LPS injection, the number of infiltrating cells, the protein concentration, and the levels of nitric oxide (NO), tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, prostaglandin (PG)-E2, monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein (MIP)-2 in the aqueous humor were determined. Immunohistochemical staining with a monoclonal antibody against activated nuclear factor (NF)-kappaB was performed to evaluate the effect of lutein on NF-kappaB activation in the iris-ciliary body (ICB) of rats. A mouse macrophage cell line (RAW264.7 cells) was stimulated with LPS in the presence or absence of lutein. Expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and degradation of inhibitor kappaB (IkappaB) were analyzed by Western blot analysis. RESULTS: Lutein suppressed the development of EIU in a dose-dependent fashion. The anti-inflammatory effect of 100 mg/kg lutein was as strong as that of 1 mg/kg dexamethasone. Treatment with lutein reduced the concentrations of NO, TNF-alpha, IL-6, PGE2, MCP-1, and MIP-2 in aqueous humor. Lutein also suppressed the activation of NF-kappaB in the ICB as well as iNOS and COX-2 expression and IkappaB degradation in RAW cells. CONCLUSIONS: These findings indicate that lutein has anti-inflammatory effects on EIU by inhibiting the NF-kappaB dependent signaling pathway and the subsequent production of proinflammatory mediators.

Animals↗
PubMed2006

Dose-ranging study of lutein supplementation in persons aged 60 years or older.

PURPOSE: To examine the dose-response relationship between oral lutein supplementation and serum lutein concentrations in persons aged 60 years and older, with or without age-related macular degeneration (AMD). METHODS: Forty-five participants with no AMD, large drusen, or advanced AMD, were randomized to receive one of three doses (2.5, 5, or 10 mg) of lutein for 6 months and to be observed for 6 additional months after the cessation of lutein supplementation. RESULTS: The mean age of the participants (33 women) was 71 years (range: 60-91). The serum lutein concentrations of each dose group were similar before supplementation, increased at 1 month, and peaked by 3 months. Median serum concentrations of the 2.5-, 5-, and 10-mg groups from baseline to month 6 increased from 18.7 to 35.1 microg/dL (2-fold increase), from 17.8 to 59.2 microg/dL (2.9-fold increase), and from 15.1 to 66.8 microg/dL (4-fold increase), respectively (all P < 0.001). The increases in lutein serum concentrations did not vary with AMD disease severity (P = 0.98). No toxicity was observed with any dose of lutein. No significant changes were detected in visual acuity or visual field tests. CONCLUSIONS: Increasing doses of lutein supplements significantly increased the serum levels of lutein and zeaxanthin, and doses up to 10 mg were safely administered. A long-term large clinical trial is necessary to investigate the safety and efficacy of lutein in reducing the risk of the development of advanced AMD.

Administration, Oral↗
PubMed1975

Transitory changes in plasma progestins, estradiol, and luteinizing hormone approaching ovulation in the bovine.

Progestins, estradiol, and luteinizing hormone were measured by radioimmunoassay in bovine plasma samples collected from indwelling jugular catheters daily on days minus 6 to minus 4, every 6 h on days minus 3 and minus 2, and every 2 h from day minus 1 to ovulation. Least squares analyses characterized time trends within animals and interrelationships between these hormones. Plasma progestins decreased from 5.7 ng/ml at day minus 6 to .07 ng at the peak of luteinizing hormone. No preovulatory peripheral increase in plasma progestins was detected. Estradiol increased from 2 pg/ml at day minus 4 to 6 pg at minus 12 h and then increased abruptly to 7.4 pg at the peak of luteinizing hormone. This matter increase in estradiol was synchronous with the acute preovulatory surge of luteinizing hormone. Association was positive between estradiol and luteinizing hormone, but negative between progestins and estradiol. Estradiol decreased 50% by 5 h following the peak of luteinizing hormone with a return to base (2 pg) at 14 h. An increase of .1 ng luteinizing hormone/ml plasma per day was linear from day minus 6 to 8 h prior to the luteinizing hormone peak. Luteinizing hormone increased to a peak of 13.5 ng/ml and remained elevated for 10.5 h. These results are consistent with the hypothesis that an increase at proestrus in estradiol rather than progestins triggers the preovulatory surge of luteinizing hormone in the bovine.

Animals↗
PubMed1986

3'-Oxolutein, a metabolite of lutein in chickens.

3'-Oxolutein (3-hydroxy-3'-oxo-beta,epsilon-carotene) was isolated using high performance liquid chromatography (HPLC) from the tissues and egg yolks of chicken 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 greater than intestinal mucosa greater than serum greater than liver approximately toe web approximately egg yolk greater than 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.

Animals↗
PubMed2002

[Expression of macrophage colony-stimulating factor in human luteinized granulosa cells].

OBJECTIVE: To detect and localize the expression of macrophage colony-stimulating factor (M-CSF) in human luteinized granulosa cells and investigate the effects of follicle stimulating hormone (FSH) on M-CSF production by human luteinized granulosa cells in vitro. METHODS: Human luteinized granulosa cells were isolated from follicular fluid of superovulated infertile patients undergoing intracytoplasmatic sperm injection. Some of the luteinized granulosa cells were used for detecting M-CSF by immunocytochemical staining (ABC method). Most of them were cultured with HAM's F-10 medium alone or plus various concentrations of FSH (2, 5, 15, 25 IU/ml). The media were collected after 72 hours and their M-CSF contents were measured by a solid phase enzyme-linked immunosorbant assay. RESULTS: About 80% of the luteinized granulosa cells were positively stained for M-CSF antibody. The immunoreactive signals of M-CSF were specially located in the cytoplasma of the luteinized granulosa cells. No immunoreactivity of M-CSF was observed in vaginal squamous epithelial cells through contaminations during transvaginal oocyte retrieval. The concentration of M-CSF in cultured luteinized granulosa cells medium without FSH stimulation was low. However, addition of 2, 5, 15, 25 IU/ml concentrations of FSH caused significant dose-dependent increases of M-CSF production after 72 hours culture by luteinized granulosa cells (P < 0.01). CONCLUSIONS: Human luteinized granulosa cells can synthesize and secrete M-CSF. FSH can directly stimulate M-CSF secretion by human luteinized granulosa cells. The mechanism of FSH regulating follicular development may partially via M-CSF/receptor pathway.

Adult↗
PubMed2003

Atmospheric pressure chemical ionization mass spectrometry and in-source fragmentation of lutein esters.

Negative-ion atmospheric pressure chemical ionization (APCI) mass spectrometry and in-source collisionally induced dissociation (CID) were employed to obtain structural information of lutein esters from marigold extract. Both molecular ions and structurally significant fragments corresponding to the loss of fatty acids were observed in high abundance in the current study. Six lutein diesters including lauroylmyristoyl-lutein (LML), dimyristoyl-lutein (dML), myristoylpalmitoyl-lutein (MPL), dipalmitoyl-lutein (dPL), palmitoylstearoyl-lutein (PSL) and distearoyl-lutein (dSL) were characterized in a marigold flower extract. Breakdown curves (plots of relative ion abundance vs. internal energy) of three lutein diesters were established by monitoring the relative ion abundance of molecular and fragment ions at different cone voltages during negative-ion APCI-LC/MS analysis.

Atmospheric Pressure↗
PubMed2000

Use of a 13C tracer to quantify the plasma appearance of a physiological dose of lutein in humans.

Increased intake of lutein from vegetables promotes increased density of the macular pigment and therefore may protect against age-related macular degeneration. Our objective was to use a 13C tracer and high-precision gas chromatography-combustion interfaced-isotope ratio mass spectrometry (GC-C-IRMS) to investigate metabolism of a lutein dose equivalent to that absorbed from vegetables. Biosynthetic per-labeled (>99% 13C) lutein was purified from a commercially available extract of algal biomass. Subjects (n = 4) ingested 3 mg of [13C]lutein with a standardized low-carotenoid breakfast. Blood samples were collected at baseline and then hourly for 12 h; additional blood samples were drawn at 16, 24, 48, 72, 96, 192, 360, and 528 h. To produce perhydro-beta-carotene suitable for analysis by GC-C-IRMS, the plasma lutein fraction was hydrogenated on palladium-on-carbon catalyst with acid-catalyzed hydrogenolysis. The stable carbon isotope (13C/12C) ratio measured by GC-C-IRMS was used to calculate the plasma concentration of [13C]lutein. There was a rapid increase in [13C]lutein in plasma until peak enrichment at 16 h followed by a decline to the next measurement at 24 h. At 528 h, small changes in 13C enrichment from baseline could still be measured in plasma lutein. High-precision GC-C-IRMS enables complete definition of the appearance and disappearance of [13C]lutein in plasma after ingestion of a dose similar to that absorbed from foods.

Adult↗
PubMed2005

Use of a 13C tracer to investigate lutein as a ligand for plasma transthyretin in humans.

The selective accumulation of lutein in the macula of the human retina is likely to be mediated by specific transport and/or binding proteins. Our objective was to determine whether transthyretin (TTR) is a plasma transport protein for lutein. We used a biosynthetic 13C-lutein tracer and GC-combustion interfaced-isotope ratio MS to gain the requisite sensitivity to detect the minute amounts of lutein expected as a physiological ligand for TTR. Subjects (n = 4) each ingested 1 mg of 13C-lutein daily for 3 d and donated blood 24 h after the final dose. For three subjects, the plasma TTR-retinol-binding protein (RBP) complex was partially purified by anion-exchange (diethylaminoethyl, DEAE) chromatography and then dissociated by hydrophobic-interaction chromatography to yield the TTR component. For subject 4, the initial DEAE purification step was omitted and total plasma TTR (RBP-bound and free) was isolated by hydrophobic-interaction chromatography. In each case, the crude TTR fractions were then purified to homogeneity by RBP-Sepharose affinity chromatography. Pure TTR was extracted with chloroform, and unlabeled lutein was added to the extract as a carrier. The mean 13C/12C ratio (expressed in delta notation, delta13C) of the lutein fraction isolated from the plasma TTR extracts of the four subjects was -30.53 +/- 3.29 per thousand. The delta13C value of the unlabeled lutein carrier was -30.97 +/- 0.27per thousand. Thus, no 13C enrichment was detected in association with TTR. We conclude that lutein is not associated with TTR in human plasma after being ingested in physiological amounts.

Administration, Oral↗
PubMed1988

Low-dose dopamine infusions do not ablate luteinizing hormone pulses in women.

The effect of dopamine on the secretion of luteinizing hormone in 15 euprolactinemic and 15 hyperprolactinemic women was investigated using infused doses of dopamine that achieved circulating levels from 2 to 100 times basal physiologic concentrations. The normal women were studied in the early follicular phase of the cycle. Different concentrations of dopamine were maintained at each dose level for 2 hours. Blood samples were obtained every 15 minutes and concentrations of dopamine, luteinizing hormone, follicle-stimulating hormone, and prolactin quantified. Mean basal concentrations of estradiol were 53 +/- 19 pg/ml in the euprolactinemic and 33 +/- 12 pg/ml in the hyperprolactinemic women; mean prolactin levels were 8.1 +/- 3.9 ng/ml in euprolactinemic and 183 +/- 174 ng/ml in hyperprolactinemic women; mean basal dopamine concentrations were 323 +/- 308 pg/ml in euprolactinemic and 337 +/- 232 pg/ml in hyperprolactinemic women. All doses of dopamine achieved some degree of prolactin suppression, but doses that achieved nanomolar circulating concentrations did not significantly affect luteinizing hormone secretion. Eight of the women in each group exhibited high-amplitude luteinizing hormone pulses, which persisted during the dopamine infusions. Neither the amplitude nor frequency of luteinizing hormone release correlated with basal estradiol, luteinizing hormone, or prolactin levels. We conclude that low doses of dopamine infused into the peripheral circulation do not achieve significant suppression of luteinizing hormone release. In some women during the early follicular phase of the menstrual cycle and in some amenorrheic hyperprolactinemic women, luteinizing hormone is secreted in a pulsatile manner characterized by high-amplitude low-frequency bursts. These bursts of luteinizing hormone were not influenced by elevations in circulating dopamine concentrations sufficient to suppress prolactin.

Adult↗
PubMed2000

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 10mg 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 10mg lutein. Concentrations of plasma retinol and alpha-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 10mg lutein on Weeks 8 and 12. These results support the immuno-modulatory action of lutein in domestic cats.

Animals↗
PubMed2000

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+/-0.4kg body weight) were supplemented daily with 0, 5, 10 or 20mg 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.

Adjuvants, Immunologic↗
PubMed2004

NMDA receptors in the medial zona incerta stimulate luteinizing hormone and prolactin release.

1. The aim of the present work is to demonstrate the interaction between the glutamatergic/NMDA and dopaminergic systems in the medial zona incerta on the control of luteinizing hormone and prolactin secretion and the influence of reproductive hormones. 2. Proestrus and ovariectomized rats were primed with estrogen and progesterone to induce high or low levels of luteinizing hormone and prolactin. 2-Amino-7-phosphonoheptanoic acid, an NMDA receptor antagonist, and dopamine were injected in the medial zona incerta. Blood samples were withdrawn every hour between 1,600 and 2,000 hours or 2,200 hours via intracardiac catheter from conscious rats. Additional groups of animals injected with the NMDA receptor antagonist were killed 1 or 4 h after injection. Dopamine and its metabolite 3,4-dihydroxyphenylacetic acid were measured in different hypothalamic regions. 3. 2-Amino-7-phosphonoheptanoic acid blocked the ovulatory luteinizing hormone surge in proestrus rats. 2-Amino-7-phosphonoheptanoic acid also blocked the increase in luteinizing hormone induced by ovarian hormones in ovariectomized rats, an effect that was partially reversed by dopamine injection. Conversely, the increased release of luteinizing hormone and prolactin induced by dopamine was prevented by 2-amino-7-phosphonoheptanoic acid. We found that the NMDA antagonist injection decreased the dopaminergic activity--as evaluated by the 3,4-dihydroxyphenylacetic acid/dopamine ratio--in the medio basal hypothalamus and increased in the preoptic area. 4. Our results show an stimulatory role of NMDA receptors on the ovulatory luteinizing hormone release and on luteinizing hormone release induced by sexual hormones and demonstrate that the stimulatory effect of dopamine on luteinizing hormone and prolactin is mediated by the NMDA receptors. These results suggest a close interaction between the glutamatergic and dopaminergic incertohypothalamic systems on the control of luteinizing hormone and prolactin release.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Fruits and vegetables that are sources for lutein and zeaxanthin: the macular pigment in human eyes.

BACKGROUND: It has been suggested that eating green leafy vegetables, which are rich in lutein and zeaxanthin, may decrease the risk for age related macular degeneration. The goal of this study was to analyse various fruits and vegetables to establish which ones contain lutein and/or zeaxanthin and can serve as possible dietary supplements for these carotenoids. METHODS: Homogenates of 33 fruits and vegetables, two fruit juices, and egg yolk were used for extraction of the carotenoids with hexane. Measurement of the different carotenoids and their isomers was carried out by high performance liquid chromatography using a single column with an isocratic run, and a diode array detector. RESULTS: Egg yolk and maize (corn) contained the highest mole percentage (% of total) of lutein and zeaxanthin (more than 85% of the total carotenoids). Maize was the vegetable with the highest quantity of lutein (60% of total) and orange pepper was the vegetable with the highest amount of zeaxanthin (37% of total). Substantial amounts of lutein and zeaxanthin (30-50%) were also present in kiwi fruit, grapes, spinach, orange juice, zucchini (or vegetable marrow), and different kinds of squash. The results show that there are fruits and vegetables of various colours with a relatively high content of lutein and zeaxanthin. CONCLUSIONS: Most of the dark green leafy vegetables, previously recommended for a higher intake of lutein and zeaxanthin, have 15-47% of lutein, but a very low content (0-3%) of zeaxanthin. Our study shows that fruits and vegetables of various colours can be consumed to increase dietary intake of lutein and zeaxanthin.

Carotenoids↗
PubMed2006

Lutein supplementation in retinitis pigmentosa: PC-based vision assessment in a randomized double-masked placebo-controlled clinical trial [NCT00029289].

BACKGROUND: There is no generally accepted medical or surgical treatment to stop the progressive course of retinitis pigmentosa. Previous studies have suggested lutein as a potential treatment with positive effects on macular pigment density. The objective of this study was to examine the effect of lutein supplementation on preservation of visual function in patients with retinitis pigmentosa (RP) METHODS: In a double-masked randomized placebo-controlled phase I/II clinical trial with a cross-over design, 34 adult patients with RP were randomized to two groups. One group, consisted of 16 participants, received lutein supplementation (10 mg/d for 12 wks followed by 30 mg/d) for the first 24 weeks and then placebo for the following 24 weeks, while the other group included 18 participants for whom placebo (24 weeks) was administered prior to lutein. Visual acuity, contrast sensitivity, and central visual field were measured at different illumination levels at baseline and every week using a PC-based test at home. RESULTS: For visual acuity (VA) at normal illumination level, treatment with lutein reduced logMAR, i.e. improved VA, but this effect was not statistically significant. The changes in normal (100%), low (4%), and very low (0.1%) illumination log CS were not statistically significant (p-values: 0.34, 0.23, and 0.32, respectively). Lutein had a statistically significant effect on visual field (p-value: 0.038) and this effect increased in the model assuming a 6-week delay in effect of lutein. Comparing the development of vision measures against the natural loss expected to occur over the course of 48 weeks, most measures showed reduced decline, and these reductions were significant for normal illumination VA and CS. CONCLUSION: These results suggest that lutein supplementation improves visual field and also might improve visual acuity slightly, although these results should be interpreted cautiously. As a combined phase I and II clinical trial, this study demonstrated the efficacy and safety of lutein supplementation.

Contrast Sensitivity↗
PubMed1998

Possible involvement of transforming growth factor-beta 1 and transforming growth factor-beta receptor type II during luteinization in the marmoset ovary.

The expression of transforming growth factor-beta 1 (TGF-beta 1), and transforming growth factor-beta receptor type II (T beta R-II), were evaluated in periovulatory marmoset ovaries. Histochemical methods were used, in particular double-labelling techniques, in order to correlate growth factor/receptor expression with proliferation (Ki 67), apoptosis (TUNEL method) and luteinization (3 beta-hydroxysteroid dehydrogenase (3 beta-HSD)). The latter was used as a luteinization marker. Periovulatory ovaries are especially suited for studying all aspects since they typically consist of small non-luteinized follicles, large luteinizing follicles and corpora lutea accessoria (Clas), which have developed from large luteinizing follicles. TGF-beta 1 and T beta R-II expression was found in luteinizing theca cells of large periovulatory follicles and in all luteal cells of Clas. Non-luteinized theca cells, including those of small follicles were always devoid of any immunostaining. Granulosa cells of small follicles were immunopositive for T beta R-II. Large follicles with granulosa cell immunoreactivity of both antibodies coexisted with non-reactive follicles of comparable size. The highest activity of the luteal marker enzyme 3 beta-HSD was co-localized in the same cells that expressed TGF-beta 1 and T beta R-II. The double-labelling experiments revealed that TGF-beta 1 and T beta R-II expression is not correlated with proliferation or apoptosis of follicular cells. Our results indicate that TGF-beta 1 and T beta R-II participate in differentiation processes, i.e. luteinization, rather than proliferation. In particular, the dynamics of T beta R-II expression appear highly related to the process of luteinization.

3-Hydroxysteroid Dehydrogenases↗
PubMed2002

Concentration of vascular endothelial growth factor released by cultured human luteinized granulosa cells is higher in women with polycystic ovaries than in women with normal ovaries.

To test the hypothesis that increased serum levels of vascular endothelial growth factor (VEGF) in women with polycystic ovaries or the polycystic ovary syndrome (PCOS) result from excess release by ovarian granulosa cells. Prospective study. Academic research setting. Twenty women undergoing IVF treatment, of whom 10 had normal ovaries and 10 had polycystic ovaries. Human granulosa lutein cells were isolated from follicular fluid obtained on the day of oocyte retrieval. Release of VEGF was assessed after co-incubation of granulosa lutein cells with gonadotropins and insulin. Serum and follicular fluid concentrations of VEGF were measured. Release of VEGF from granulosa lutein cells and serum levels of VEGF. Incubation with human hCG, and luteinizing hormone increased release of VEGF into the culture medium. Insulin alone did not increase release of VEGF, but addition of insulin increased hCG-stimulated release of VEGF. Serum and follicular fluid VEGF concentrations and the amount VEGF released from granulosa lutein cells obtained from women with polycystic ovaries or PCOS and those who developed the ovarian hyperstimulation syndrome were greater than those from granulosa lutein cells obtained from women with normal ovaries and those who did not develop the ovarian hyperstimulation syndrome. The amount of VEGF released by granulosa lutein cells is gonadotropin dependent and is augmented by insulin. The increased circulating concentrations of VEGF in women with PCOS may not only be due to an increased number of actively secreting granulosa lutein cells but also due to increased secretory capacity of each granulosa cell.

Adult↗