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PubMed1984

Effects of luteinizing hormone on phosphoinositide metabolism in rat granulosa cells.

Rat granulosa cells isolated from mature Graafian follicles were incubated with luteinizing hormone under various conditions in order to follow the synthesis and degradation of phospholipids. During acute incubations, luteinizing hormone provoked rapid and concentration-dependent increases in the incorporation of 32PO4 into phosphatidic acid, phosphatidylinositol, and the polyphosphoinositides. Similarly, luteinizing hormone provoked increases in labeling of phosphatidylinositol and the polyphosphoinositides when granulosa cells were incubated with myo-[2-3H]inositol. When granulosa cells were prelabeled with 32PO4 in order to label phosphatidylinositol to constant specific radioactivity (4 h), luteinizing hormone treatment significantly increased 32P-phosphatidylinositol levels (23%). Comparable increases (27%) in the cellular concentrations of phosphatidylinositol were observed in response to luteinizing hormone. In pulse-chase experiments employing 32PO4 - or [3H]inositol-prelabeled cells, luteinizing hormone did not alter phospholipid degradation. In addition, luteinizing hormone did not stimulate degradation of polyphosphoinositides. These results demonstrate that: (a) luteinizing hormone has selective effects on phospholipid metabolism in rat granulosa cells which involve phosphatidic acid, phosphatidylinositol, and the polyphosphoinositides, (b) luteinizing hormone increases net levels of phosphatidylinositol and presumably phosphatidic acid and the polyphosphoinositides, and (c) luteinizing hormone does not increase phospholipid degradation. Our findings suggest that luteinizing hormone provokes increases in de novo synthesis of phosphatidylinositol in rat granulosa cells. These changes in phospholipid metabolism may be important for steroidogenesis and other enzymatic processes during treatment with luteinizing hormone.

Animals↗
PubMed1997

Identification of lutein and zeaxanthin oxidation products in human and monkey retinas.

PURPOSE: To characterize fully all the major and minor carotenoids and their metabolites in human retina and probe for the presence of the oxidative metabolites of lutein and zeaxanthin. METHODS: Carotenoids of a composite of 58 pairs of human retinas and a monkey retina were elucidated by comparing their high-performance liquid chromatography (HPLC)-ultraviolet/visible absorption spectrophotometry (UV/Vis)-mass spectrometry (MS) profile with those of authentic standards prepared by organic synthesis. RESULTS: In addition to lutein and zeaxanthin, several oxidation products of these compounds were present in the extracts from human retina. A major carotenoid resulting from direct oxidation of lutein was identified as 3-hydroxy-beta, epsilon-caroten-3'-one. Minor carotenoids were identified as: 3'-epilutein, epsilon,epsilon-carotene-3,3'-diol, epsilon,epsilon-carotene-3,3'-dione, 3'-hydroxy-epsilon,epsilon-caroten-3-one, and 2,6-cyclolycopene-1,5-diol. Several of the geometric isomers of lutein and zeaxanthin were also detected at low concentrations. These were as follows: 9-cis-lutein, 9'-cislutein, 13-cis-lutein, 13'-cis-lutein, 9-cis-zeaxanthin, and 13-cis-zeaxanthin. Similar results were also obtained from HPLC analysis of a freshly dissected monkey retina. CONCLUSIONS: Lutein, zeaxanthin, 3'-epilutein, and 3-hydroxy-beta,epsilon-caroten-3'-one in human retina may be interconverted through a series of oxidation-reduction reactions similar to our earlier proposed metabolic transformation of these compounds in humans. The presence of the direct oxidation product of lutein and 3'-epilutein (metabolite of lutein and zeaxanthin) in human retina suggests that lutein and zeaxanthin may act as antioxidants to protect the macula against short-wavelength visible light. The proposed oxidative-reductive pathways for lutein and zeaxanthin in human retina, may therefore play an important role in prevention of age-related macular degeneration and cataracts.

Animals↗
PubMed1987

Specific luteinizing-hormone-releasing hormone receptor binding sites in hippocampus and pituitary: an autoradiographical study.

Using the iodinated luteinizing-hormone-releasing hormone analogue [D-Ala6, N alpha MeLeu7, Pro9 NEt]-luteinizing-hormone-releasing hormone as radioligand, specific binding sites have been visualized in the rat both in the pituitary and the hippocampal formation of the brain. In the hippocampus, the CA1, CA2 and particularly CA3 regions were heavily labelled. These hippocampal sites have a pharmacological specificity resembling that of luteinizing-hormone-releasing hormone receptors in pituitary homogenates and could therefore represent true luteinizing-hormone-releasing hormone receptors. The luteinizing-hormone-releasing hormone superagonist [D-Ala6, Pro9 NEt]-luteinizing-hormone-releasing hormone and the potent antagonist [D-pGlu1, D-Phe2, D-Trp3,6]-luteinizing-hormone-releasing hormone were highly potent in displacing the iodinated luteinizing-hormone-releasing hormone analogue. The weak agonist [Gln8]-luteinizing-hormone-releasing hormone, however, was at least two orders of magnitude less potent. Somatostatin was inactive. Hippocampal luteinizing-hormone-releasing hormone receptors were species-specific, being present in the rat but not in the mouse, guinea-pig, hamster, rabbit and human brains. In order to identify the cellular location of these hippocampal receptors, various lesions were performed. Electrolytic lesions of the septal afferents did not reveal any receptor density change. Colchicine as well as kainic acid injections did, however, reduce considerably the number of hippocampal receptors. Interestingly, in the electrolytically and kainic-acid-lesioned animals, the appearance of non-displaceable luteinizing-hormone-releasing hormone binding sites within a well-defined area corresponding to the lesioned, gliosis-rich area was observed. The present results suggest the presence of pharmacologically specific, species-dependent, luteinizing-hormone-releasing hormone receptors located, at least partly, on intrinsic hippocampal neurons, in particular granule and pyramidal cells.

Animals↗
PubMed2002

Antitumor effects of the cytotoxic luteinizing hormone-releasing hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.

OBJECTIVE: Most human endometrial and ovarian cancers express receptors for luteinizing hormone- releasing hormone. These receptors can be used for targeted chemotherapy with cytotoxic luteinizing hormone-releasing hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys(6)]luteinizing hormone-releasing hormone. STUDY DESIGN: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human luteinizing hormone-releasing hormone receptor-positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the luteinizing hormone-releasing hormone receptor-negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing hormone-releasing hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase-polymerase chain reaction and radioligand binding assay. RESULTS: The tumor volumes of luteinizing hormone-releasing hormone receptor-positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly (P <.001) 1 week after treatment with AN-152 at 700 nmol/20 g or at 300 nmol/20 g. No toxic side effects were observed. Treatment with doxorubicin arrested tumor growth but did not reduce tumor volume. Doxorubicin at 700 nmol/20 g caused a high mortality rate and at 300 nmol/20 g (8.7 mg/kg) caused a loss of body weight, but no deaths occurred. The growth of luteinizing hormone-releasing hormone receptor-negative SK-OV-3 cancers was not affected by AN-152. Normal human nonreproductive tissues, hematopoietic stem cells, and vaginal tissue did not express luteinizing hormone-releasing hormone receptors, but luteinizing hormone-releasing hormone receptors were found in the ovary, fallopian tube, cervix, endometrium, and myometrium. CONCLUSION: Targeted chemotherapeutic luteinizing hormone-releasing hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on luteinizing hormone-releasing hormone receptor-positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers.

Animals↗
PubMed1990

Antiprogestin treatment decreases midluteal luteinizing hormone pulse amplitude and primarily exerts a pituitary inhibition.

Mifepristone (RU 486), a synthetic steroid with antiprogesterone receptor activity, was given with and without naloxone hydrochloride to six women in the midluteal phase to investigate the role of progesterone in the modulation of endogenous opioid activity and the secretion of luteinizing hormone and cortisol. Subjects were evaluated during four sequential monthly admissions during which multiple blood samples were obtained every 15 minutes for 8 hours. Patients were studied during a baseline cycle, after administration of RU 486 alone (100 mg/day), naloxone with RU 486, and naloxone alone. After administration of RU 486 there was a significant decline in total luteinizing hormone secretion (p less than 0.01) and luteinizing hormone pulse amplitude (p less than 0.05), but compared with baseline there was no significant change in luteinizing hormone pulse frequency. After infusion of naloxone there was a significant increase in mean luteinizing hormone values (p less than 0.05) and luteinizing hormone pulse frequency (p less than 0.01) but no change in pulse amplitude. There was no significant difference in mean luteinizing hormone values or luteinizing hormone pulse amplitude and frequency between administration of RU 486 and naloxone plus RU 486. Administration of naloxone alone, RU 486 alone, and RU 486 plus naloxone caused a significant increase in cortisol as compared with baseline cycles (p less than 0.05). These data further support the notion that progesterone is important in the control of luteinizing hormone secretion and suggest that progesterone may primarily influence luteinizing hormone pulse amplitude and pituitary release of luteinizing hormone during the luteal phase.

Adult↗
PubMed2002

Macular pigment density in relation to serum and adipose tissue concentrations of lutein and serum concentrations of zeaxanthin.

BACKGROUND: Macular pigment (MP), concentrated in the central area of the retina, contains the carotenoids lutein and zeaxanthin. A low MP density could be a risk factor for age-related macular degeneration. Little information is available regarding MP density in relation to serum lutein and zeaxanthin and adipose lutein concentrations in a general population. OBJECTIVE: The objective was to investigate the associations between MP density and serum lutein, serum zeaxanthin, and adipose lutein, taking into account potential confounders in a population. DESIGN: Volunteers (n = 376) aged 18-75 y were recruited. In a cross-sectional design, serum (n = 376) and adipose tissue (n = 187) were analyzed for carotenoids, and MP density was measured by spectral fundus reflectance. RESULTS: Mean MP density in the total study group was 0.33 +/- 0.15. MP density was 13% higher in men than in women (P < 0.05). Serum and blood concentrations of alpha-tocopherol, vitamin C, and all carotenoids except lycopene were significantly higher in women. Adipose lutein concentrations were also significantly higher in women than in men. Regression models showed a positive significant association between MP density and serum lutein, serum zeaxanthin, and adipose lutein concentrations in men after adjustment for age, but no relation in women. In men, serum lutein remained significantly associated with MP density after adjustment for age, total cholesterol, body mass index, and smoking. CONCLUSION: The associations between MP density and serum lutein, serum zeaxanthin, and adipose lutein concentrations are stronger in men than in women.

Adipose Tissue↗
PubMed2002

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.

Adolescent↗
PubMed2006

Dietary lutein and fat interact to modify macrophage properties in chicks hatched from carotenoid deplete or replete eggs.

Two experiments were conducted to study the interaction between dietary lutein and fat levels in broiler chicks hatched from lutein depleted (Experiment I) and repleted (Experiment II) eggs. In both experiments, a 2 x 3 factorial arrangement of treatments resulted in six dietary treatments (fat at 3% and 6% and lutein at 0, 25 and 50 mg/kg feed) that were fed for 23 days to 18 birds per treatment (in three replications). In Experiment I, the anti-dinitrophenyl-keyhole-lympet-hemocyanin (anti-DNP-KLM) serum antibody response at day 22 and macrophage phagocytotic index at day 17 did not differ among treatment groups (p > 0.05). The concavalin A and phytohaemagglutinin-P lymphocyte proliferation index at day 19 was greater in birds fed 50 mg of lutein and 3% fat than in birds fed all other diets (p < 0.05). Independent of the level of dietary fat, dietary lutein increased macrophage (day 23) nitrite production measured 46 h after in vitro stimulation with LPS (p < 0.05). Among the birds fed lutein at 25 or 50 mg/kg feed, birds fed 3% fat had higher LPS-induced nitrite production compared to the birds fed 6% fat after 46 (p = 0.014) or 70 h (p < 0.001). In Experiment II, macrophage nitrite production was measured at 54 h after LPS stimulation on days 11, 15, 19 and 23. An interaction between dietary lutein and fat levels on nitrite production was observed on day 19 (p = 0.012), where macrophages from birds fed 0 mg lutein and 3% fat had the highest nitrite production (p = 0.012). Macrophages from birds fed lutein at 25 and 50 mg/kg diet and 3% fat had higher (p = 0.012) nitrite production than birds fed 6% fat. Thus, in birds hatched from lutein deplete and replete eggs, modulation of macrophage nitrite production by lutein is dependent on the level of dietary fat.

Animals↗
PubMed2001

Oxygenated carotenoid lutein and progression of early atherosclerosis: the Los Angeles atherosclerosis study.

BACKGROUND: Carotenoids are hypothesized to explain some of the protective effects of fruit and vegetable intake on risk of cardiovascular disease. The present study assessed the protective effects of the oxygenated carotenoid lutein against early atherosclerosis. METHODS AND RESULTS EPIDEMIOLOGY: Progression of intima-media thickness (IMT) of the common carotid arteries over 18 months was determined ultrasonographically and was related to plasma lutein among a randomly sampled cohort of utility employees age 40 to 60 years (n=480). Coculture: The impact of lutein on monocyte response to artery wall cell modification of LDL was assessed in vitro by quantification of monocyte migration in a coculture model of human intima. Mouse models: The impact of lutein supplementation on atherosclerotic lesion formation was assessed in vivo by assigning apoE-null mice to chow or chow plus lutein (0.2% by weight) and LDL receptor-null mice to Western diet or Western diet plus lutein. IMT progression declined with increasing quintile of plasma lutein (P for trend=0.007, age-adjusted; P=0.0007, multivariate). Covariate-adjusted IMT progression (mean+/-SEM) was 0.021+/-0.005 mm in the lowest quintile of plasma lutein, whereas progression was blocked in the highest quintile (0.004+/-0.005 mm; P=0.01). In the coculture, pretreatment of cells with lutein inhibited LDL-induced migration in a dose-dependent manner (P<0.05). Finally, in the mouse models, lutein supplementation reduced lesion size 44% in apoE-null mice (P=0.009) and 43% in LDL receptor-null mice (P=0.02). CONCLUSIONS: These epidemiological, in vitro, and mouse model findings support the hypothesis that increased dietary intake of lutein is protective against the development of early atherosclerosis.

Adult↗
PubMed2005

Storage stability of lutein during ripening of cheddar cheese.

Lutein (3,3'-dihydroxy-alpha-carotene) has been identified as a dietary factor that can delay the onset of age-related macular degeneration (AMD). However, available food sources of lutein contain only modest amounts of the carotenoid. Food fortification with lutein extract has been identified as a low-budget approach to prevent the onset or progression of AMD. The objectives of this study were to 1) incorporate various amounts of lutein into Cheddar cheese; 2) examine the color, pH, microbiological, and sensory characteristics of the Cheddar cheese during storage; and 3) analyze the stability of lutein during the cheese maturation process. Lutein extracted from corn was added to Cheddar cheese in quantities of 1, 3, and 6 mg per serving size. Measurements of the lutein stability were carried out by HPLC using a YMC C30 carotenoid column. Microbiological analyses of cheese samples included aerobic plate count, coliform, and yeast/mold counts. The color attributes a* and b* were significantly different between the treatment and control groups; however, no significant difference was observed in L* value and pH. Significant differences among 1, 3, and 6 mg lutein-enriched cheeses were observed in the aerobic plate count and yeast/mold compared with the control. Cheese samples contained no detectable levels of coliforms (< 10 cfu/g). The HPLC data showed quantitative recovery of lutein during the storage period, and no lutein degradation products were identified. These results indicate that lutein, a functional additive with purported ability to prevent or reduce the onset of AMD, can be incorporated into cheese adding value to this product.

Cheese↗
PubMed1986

Lutein as a model dihydroxycarotenoid for the study of pigmentation in chickens.

A model for the study of pigmentation in young chickens is described in which a white corn-soy based diet supplemented with varying amounts of free lutein (0, 5, 10, 20, 40, and 80 micrograms/g diet) was fed from hatching until 3 weeks of age. The carotenoid content of tissues dissected from chicks of the various groups was measured by high pressure liquid chromatography. In intestinal contents, three forms of lutein were found, with lutein monoester greater than free lutein greater than lutein diester. In the serum, free lutein (96%) and lutein monoester (4%) were found. In the liver, free lutein (80%), monoester (20%), and traces of diester were found. In the integument (toe web), diester greater than monoester approximately equal to free alcohol were found. In each tissue, the concentrations were directly proportional to the dietary concentration of free lutein. The simplest explanation of the data appears to be that part of the free lutein in the diet is esterified during its passage down the intestinal tract and, regardless of its status when absorbed, it is transported in the body as the free alcohol. When it enters depot sites such as the integument, lutein is deposited mainly as esters, presumably as the result of local enzymatic activity.

Animals↗
PubMed1987

Aging changes in synaptology of luteinizing hormone-releasing hormone neurons in male rat preoptic area.

This study was undertaken to examine some aspects of the anatomical substrate for reproductive senescence. Immunocytochemically identified luteinizing hormone-releasing hormone neurons and their processes in the male rat brain preoptic area were compared in young adult (2-4 months), middle-aged (12-14 months) and old (20-23 months) animals. At the light microscopic level there were no age-dependent differences in total numbers or sizes of LHRH neurons nor in their distribution in the brain. Examination of these neurons at the electron microscopic level did reveal significant differences in certain organelles and in the degree and kind of synaptic input. Random sections of middle-aged luteinizing hormone-releasing hormone neurons more frequently passed through the nucleolus and the incidence of nematosomes was higher than in luteinizing hormone-releasing hormone neurons from the young and old animals. Quantitative measures of synaptic input to luteinizing hormone-releasing hormone soma and dendrites as well as to unidentified neurons in the same thin section were made. These are reported as percent of membrane that showed synaptic structure. Dendrites of both luteinizing hormone-releasing hormone and nonidentified neurons were more densely innervated than perikarya. The density of synaptic input to luteinizing hormone-releasing hormone neurons was significantly greater than that to nonidentified neurons in young and middle-aged animals, but was equal to that of nonidentified neurons by old age. Age-related changes were noted in synaptic organization with the most significant change being an increased input to luteinizing hormone-releasing hormone perikarya. Indeed, synaptic input to luteinizing hormone-releasing hormone perikaryal membrane was increased three-fold by middle age and ten-fold by old age. Density of synaptic input to luteinizing hormone-releasing hormone dendritic membrane did not change with age. There were no aging changes in percentage of membrane with synaptic structure in nonidentified elements. Synapses were also classified on the basis of their synaptic vesicle content. There were proportionately more synaptic boutons containing round clear than pleomorphic vesicles in the young sample. The proportion of synapses with pleomorphic vesicles increased with age onto both luteinizing hormone-releasing hormone perikarya and their dendrites. The proportion of boutons containing some electron dense-core vesicles along with clear vesicles decreased with age onto both luteinizing hormone-releasing hormone and nonidentified neurons and their processes.

Aging↗
PubMed1986

Histologic and hormonal documentation of the luteinized unruptured follicle syndrome.

Histologic and hormonal documentation of a luteinized unruptured follicle that occurred during a spontaneous menstrual cycle in a rhesus monkey is presented. Frequent (every 2 hours) blood sampling to assess midcycle hormonal dynamics in the monkey with the luteinized unruptured follicle and in five monkeys with an ovulatory stigma revealed significant aberrations in the gonadotropin and steroid hormone profiles associated with a luteinized unruptured follicle. Although the midcycle 17 beta-estradiol surge was normal, the monkey with the luteinized unruptured follicle demonstrated (1) blunted midcycle bioassayable luteinizing hormone, immunoassayable luteinizing hormone, and follicle-stimulating hormone surges; (2) absence of disparity in the bioassayable luteinizing hormone: immunoassayable luteinizing hormone ratio during the gonadotropin surge; (3) absence of progesterone and 17 alpha-hydroxyprogesterone secretion during the gonadotropin surge; and (4) delayed and blunted rise in progesterone and 17 alpha-hydroxyprogesterone after the gonadotropin surge. These findings suggest that an impaired luteinizing hormone surge, perhaps mediated by insufficient midcycle progestin secretion, is one possible cause of the luteinized unruptured follicle syndrome.

17-alpha-Hydroxyprogesterone↗
PubMed1991

The induction of premature luteolysis in normal women--follicular phase luteinizing hormone secretion and corpus luteum function in the subsequent cycle.

Women with luteal phase deficiency have been shown to have an increased frequency of luteinizing hormone pulses in the early follicular phase of the menstrual cycle. Because progesterone is known to modulate luteinizing hormone secretion, it has been hypothesized that the decreased progesterone secretion in a previous luteal phase deficiency cycle could lead to the abnormal luteinizing hormone secretory pattern in the ensuing early follicular phase. With the possibility that the higher luteinizing hormone pulse frequency might lead to another deficient luteal phase, it becomes conceivable that luteal phase deficiency could be self-perpetuating. To test this hypothesis, luteal phase deficiency was induced in six normal women by decreasing luteinizing hormone support of the corpus luteum with a gonadotropin-releasing hormone antagonist Nal-Glu, administered twice daily beginning in the midluteal phase after a control cycle. During the antagonist-treated luteal phase, each subject met the predetermined criteria for induced luteal phase deficiency: a 33% or greater decrease in integrated progesterone from the control cycle and an integrated progesterone level less than 100 ng/ml per day. Luteinizing hormone secretion patterns were determined by frequent blood sampling performed every 10 minutes for 12 hours in the early follicular phase of the control cycle and the cycle after antagonist administration. Daily luteal progesterone levels were measured in the control, treatment, and posttreatment cycles. Each volunteer served as her own control. Standard parameters were compared between the control and posttreatment pulse studies in the early follicular phase: (1) luteinizing hormone pulse frequency was 9.5 +/- 1.0 vs 10.0 +/- 0.9 pulses/12 hours, control vs posttreatment, respectively, p = 0.5; (2) luteinizing hormone pulse amplitude was 11.0 +/- 1.3 vs 12.0 +/- 2.2 ng/ml, p = 0.6; and (3) luteinizing hormone mean level was 19.4 +/- 2.3 vs 22.2 +/- 3.3 ng/ml, p = 0.1. Corpus luteum function was also compared between the control and posttreatment cycles. Luteal phase length was 13.7 +/- 0.6 vs 12.7 +/- 0.6 days, p = 0.08. Integrated progesterone values were 136.9 +/- 12.9 vs 130.5 +/- 11.3 ng/ml per day, p = 0.5. Therefore no discernible abnormalities in early follicular luteinizing hormone secretions or corpus luteum secretion of progesterone occurred after an induced luteal phase deficiency cycle.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2005

Lutein in selected Canadian crops and agri-food processing by-products and purification by high-speed counter-current chromatography.

This study mainly focused on lutein content in several selected crops grown in southern Ontario, Canada. Marigold flower, a good rotation crop for the control of nematodes in tobacco fields was found to contain 0.77% lutein (after saponification, on dry basis). A high-speed counter-current chromatography (HSCCC) method using a two-phase solvent system consisting of hexane-ethanol-water (6:4.5:1.5, v/v/v) was developed for the purification of lutein from the saponification mixture of marigold flower extract. The purity of lutein prepared using this HSCCC method was 97%. Free lutein was found to be the predominant form in three squash varieties, and it was mostly found in the peel rather than the commonly consumed flesh. Sweet Mamma, Buttercup and Pepper squash varieties contained 25.4, 18.4 and 30.1mg/100g fresh weigh (FW) of lutein in the peels, respectively. These concentrations were significantly higher than that in spinach and kale (3.7 and 12.3 mg/100 g FW). beta-Carotene was found most in the peel of Sweet Mamma squash at 13.6 mg/100g FW, whereas it was below 2mg/100g FW in all other samples. Cooking increased extractable free lutein by 22-65% in squash peels. Lutein in Yukon Gold potato was at ca. 0.4 mg/100 g FW. Certain Yukon Gold was also found to contain violaxanthin (0.35 mg/100 g FW). Structures of lutein, beta-carotene and violaxanthin were identified by LC-atmospheric pressure chemical ionization MS in positive ion mode, and by comparing the retention time and UV-vis spectral data with standards. Results from this study suggest the selected crops and agri-food industrial processing by-products of these can be a good source of free lutein.

Calendula↗
PubMed2006

Antioxidant activity, mutagenicity/anti-mutagenicity, and clastogenicity/anti-clastogenicity of lutein from marigold flowers.

High dietary intake of lutein has been associated with risk reduction of many chronic diseases, including age-related macular degeneration (AMD), cancer, and cardiovascular diseases. Lutein in food is generally regarded as safe. However, information on the toxicological and beneficial effect of lutein at higher doses is limited. In this study, large amount of lutein was extracted and purified from marigold flower (Tagetes erecta L.). The antioxidant activity of lutein was examined by using the photochemiluminescence (PCL) assay and the beta-carotene-linoleic acid model system (beta-CLAMS). Lutein showed a greater antioxidant activity than the other two common carotenoids, beta-carotene and lycopene. The mutagenicity and anti-mutagenicity of lutein at 334, 668 and 1335 microg/plate were examined using the standard Ames test in the presence and absence of S9 mix. Lutein was not only found to be non-mutagenic at all doses, but it showed an anti-mutagenic effect in a dose-dependent manner. Similar results were found in a chromosome aberration test using Chinese hamster ovary cells for the evaluation of clastogenicity and anti-clastogenicity of lutein at 66.8, 133.5 and 267.0 mg/L. Our findings provided scientific evidence for the safe use and health beneficial effects of lutein.

Animals↗
PubMed2003

Bioavailability of lutein in humans from intrinsically labeled vegetables determined by LC-APCI-MS.

The aim of the investigation was to assess a stable isotope method for determining the relative bioavailability of food-derived lutein in humans. Subjects were administered a single dose of deuterium-labeled carotenoids from intrinsically labeled spinach or collard green; 10 mL blood samples were drawn at various time points over a 34 days period. The vegetables had been hydroponically grown using 25 atom-% deuterated water. Lutein molecules in the vegetables were partially deuterated with a highest abundance isotopomer at M(0) + 8 (unlabeled molecular mass, M(0,) plus 8 additional mass units from 8 deuterium atoms in the molecules). This allowed labeled lutein to be distinguished from endogenous lutein in serum samples after consuming the labeled meal. The presence of labeled lutein in the circulation was determined by liquid chromatography-mass spectrometry (LC/MS) equipped with an atmospheric pressure chemical ionization (APCI) interface. The quantification of the labeled lutein in serum samples enabled the calculation of the enrichment for each time point after the dose; these values were plotted vs. time to generate absorption-clearance curves for each of the subjects. Area under the curve analyses of four different subjects (integrated over 29 days) yielded serum lutein responses of 128, 145, 149, and 262 microg-day/mg dietary lutein, following an acute dose of spinach containing 15.4, 18.8, 18.8 and 9.8 mg labeled lutein, respectively. This technique will facilitate the study of lutein bioavailability from different foods of diverse carotenoid composition and/or following various food preparation procedures.

Aged↗
PubMed1999

Vasopressin induces a luteinizing hormone surge in ovariectomized, estradiol-treated rats with lesions of the suprachiasmatic nucleus.

The luteinizing hormone surge in the female rat is the result of the integration of multiple signals within the medial preoptic area. The medial preoptic area contains gonadotropin-releasing hormone neurons that are responsible for the release of luteinizing hormone, neurons containing estrogen receptors and terminals originating from the suprachiasmatic nucleus with, for example, vasopressin as neurotransmitter. Both the medial preoptic area and suprachiasmatic nucleus are crucial for the occurrence of luteinizing hormone surges, since lesioning of either nucleus prevents pre-ovulatory and steroid-induced luteinizing hormone surges. In this study, we investigated whether vasopressin in the medial preoptic area could be the daily neuronal signal from the suprachiasmatic nucleus responsible for the timing of the luteinizing hormone surge. Vasopressin (50 ng/microl) or Ringer solution was administered by reverse microdialysis from Zeitgeber times 7.5 to 12.5 into the medial preoptic area of ovariectomized, estradiol-treated rats. The suprachiasmatic nucleus was lesioned to remove all cyclic luteinizing hormone secretion. This was evaluated by monitoring behavioral activity; animals that were arrhythmic were included in the experiments. Hourly blood samples were taken to measure plasma luteinizing hormone levels. Preoptic vasopressin administration induced a surge-like luteinizing hormone pattern in suprachiasmatic nucleus-lesioned animals, whereas constant, basal luteinizing hormone levels were found in the control animals. These data show that vasopressin, by itself, is able to trigger the luteinizing hormone surge in suprachiasmatic nucleus-lesioned rats. We propose that vasopressin is a timing signal from the suprachiasmatic nucleus responsible for the activation of the hypothalamo-pituitary-gonadal axis in the female rat.

Animals↗