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PubMed1999

Lutein and zeaxanthin concentrations in plasma after dietary supplementation with egg yolk.

BACKGROUND: The food matrix in which carotenoids are found affects their bioavailability. Lutein and zeaxanthin are abundant in egg yolks and accumulate in the macular region of the retina, where they may affect visual function. OBJECTIVE: We sought to determine whether plasma lutein and zeaxanthin concentrations are elevated after dietary supplementation with egg yolk. DESIGN: Eleven moderately hypercholesterolemic men and women consumed 2 separate baseline diets, which contained 29-33% of energy as total fat, with 20% of energy as either beef tallow or corn oil. These diets were supplemented with cooked chicken egg yolks (1.3 egg yolks/d for an intake of 10.4 MJ). Each subject consumed all 4 diets. Each diet was consumed for 4.5 wk, with a washout period of >/=2 wk between diet phases. At the end of each diet phase, fasting morning plasma samples were collected and stored for carotenoid analysis by HPLC. Commercial chicken egg yolks were analyzed for carotenoids and cholesterol. RESULTS: Egg yolk supplementation of the beef tallow diet increased plasma lutein by 28% (P < 0.05) and zeaxanthin by 142% (P < 0.001); supplementation of the corn oil diet increased plasma lutein by 50% (P < 0.05) and zeaxanthin by 114% (P < 0.001). Changes in plasma lycopene and beta-carotene were variable, with no consistent trend. Egg yolk supplementation increased plasma LDL-cholesterol concentrations by 8-11% (P < 0.05). CONCLUSIONS: Egg yolk is a highly bioavailable source of lutein and zeaxanthin. The benefit of introducing these carotenoids into the diet with egg yolk is counterbalanced by potential LDL-cholesterol elevation from the added dietary cholesterol.

Aged↗

PubMed2004

Impaired insulin-dependent glucose metabolism in granulosa-lutein cells from anovulatory women with polycystic ovaries.

BACKGROUND: Insulin resistance and hyperinsulinaemia are well-recognized characteristics of anovulatory women with polycystic ovary syndrome (PCOS) but, paradoxically, steroidogenesis by PCOS granulosa cells remains responsive to insulin. The hypothesis to be tested in this study is that insulin resistance in the ovary is confined to the metabolic effects of insulin (i.e. glucose uptake and metabolism), whereas the steroidogenic action of insulin remains intact. METHODS: Granulosa-lutein cells were obtained during IVF cycles from seven women with normal ovaries, six ovulatory women with PCO (ovPCO) and seven anovulatory women with PCO (anovPCO). Mean body mass index was in the normal range in all three groups. Granulosa-lutein cells were cultured with insulin (1, 10, 100 and 1000 ng/ml) and LH (1, 2.5 and 5 ng/ml). Media were sampled at 24 and 48 h and analysed for glucose uptake, lactate production and (48 h only) progesterone production. RESULTS: Insulin-stimulated glucose uptake by cells from anovPCO was attenuated at higher doses of insulin (100 and 1000 ng/ml) compared with that by cells from either ovPCO (P=0.02) or controls (P=0.02). Insulin and LH stimulated lactate production in a dose-dependent manner, but insulin-dependent lactate production was markedly impaired in granulosa-lutein cells from anovPCO compared with either normal (P=0.002) or ovPCO (P<0.0001). By contrast, there was no difference in insulin-stimulated progesterone production between granulosa-lutein cells from the three ovarian types. CONCLUSIONS: Granulosa-lutein cells from women with anovPCOS are relatively resistant to the effects of insulin-stimulated glucose uptake and utilization compared with those from normal and ovPCO, whilst maintaining normal steroidogenic output in response to physiological doses of insulin. These studies support the probability of a post-receptor, signalling pathway-specific impairment of insulin action in PCOS.

Adult↗

PubMed2005

Serum and follicular fluid levels of soluble Fas, soluble Fas ligand and apoptosis of luteinized granulosa cells in PCOS patients undergoing IVF.

BACKGROUND: There are limited data about the levels of soluble apoptotic factors and their modulation with therapeutic regimens in IVF cycles. The aim of the current study was to determine follicular fluid, and serum levels of soluble Fas (sFas) and soluble Fas ligand (sFasL) in PCOS patients undergoing IVF/ICSI cycles; also to investigate the effects of metformin on these factors and on apoptosis of luteinized granulosa cells. METHODS: We investigated the serum and follicular fluid levels of sFas and sFasL in patients with PCOS (n = 28) and compared them with those of the patients with infertility due to male factor (n = 12) undergoing IVF cycles. Effects of metformin therapy on these parameters and apoptosis of luteinized granulosa cells were also investigated among the patients with PCOS. RESULTS: Serum levels of sFas were significantly lower in the PCOS group compared to those in women with infertility due to male factor. Metformin therapy in PCOS patients preceding IVF cycles increased serum levels of sFas and decreased follicular fluid levels of sFasL compared to those on placebo. Follicular fluid from PCOS patients demonstrated luteinized granulosa cell DNA fragmentation in agarose gel, whereas a similar pattern was not observed among PCOS patients undergoing metformin therapy. CONCLUSION: Decreased serum levels of sFas and luteinized granulosa cell DNA fragmentation is observed in patients with PCOS undergoing IVF cycles. Metformin therapy preceding IVF demonstrates an antiapoptotic effect with increased serum levels of sFas, decreased follicular fluid levels of sFasL and prevention of luteinized granulosa cell DNA fragmentation.

Adult↗

PubMed1999

The food matrix of spinach is a limiting factor in determining the bioavailability of beta-carotene and to a lesser extent of lutein in humans.

Carotenoid bioavailability depends, amongst other factors, on the food matrix and on the type and extent of processing. To examine the effect of variously processed spinach products and of dietary fiber on serum carotenoid concentrations, subjects received, over a 3-wk period, a control diet (n = 10) or a control diet supplemented with carotenoids or one of four spinach products (n = 12 per group): whole leaf spinach with an almost intact food matrix, minced spinach with the matrix partially disrupted, enzymatically liquefied spinach in which the matrix was further disrupted and the liquefied spinach to which dietary fiber (10 g/kg wet weight) was added. Consumption of spinach significantly increased serum concentrations of all-trans-beta-carotene, cis-beta-carotene, (and consequently total beta-carotene), lutein, alpha-carotene and retinol and decreased the serum concentration of lycopene. Serum total beta-carotene responses (changes in serum concentrations from the start to the end of the intervention period) differed significantly between the whole leaf and liquefied spinach groups and between the minced and liquefied spinach groups. The lutein response did not differ among spinach groups. Addition of dietary fiber to the liquefied spinach had no effect on serum carotenoid responses. The relative bioavailability as compared to bioavailability of the carotenoid supplement for whole leaf, minced, liquefied and liquefied spinach plus added dietary fiber for beta-carotene was 5.1, 6.4, 9.5 and 9.3%, respectively, and for lutein 45, 52, 55 and 54%, respectively. We conclude that the bioavailability of lutein from spinach was higher than that of beta-carotene and that enzymatic disruption of the matrix (cell wall structure) enhanced the bioavailability of beta-carotene from whole leaf and minced spinach, but had no effect on lutein bioavailability.

Adolescent↗

PubMed2006

Consumption of one egg per day increases serum lutein and zeaxanthin concentrations in older adults without altering serum lipid and lipoprotein cholesterol concentrations.

Lutein and zeaxanthin accumulate in the macular pigment of the retina, and are reported to be associated with a reduced incidence of age-related macular degeneration. A rich source of lutein and zeaxanthin in the American diet is the yolk of chicken eggs. Thus, the objective of the study was to investigate the effect of consuming 1 egg/d for 5 wk on the serum concentrations of lutein, zeaxanthin, lipids, and lipoprotein cholesterol in individuals >60 y of age. In a randomized cross-over design, 33 men and women participated in the 18-wk study, which included one run-in and one washout period of no eggs prior to and between two 5-wk interventions of either consuming 1 egg or egg substitute/d. Serum lutein 26% (P < 0.001) and zeaxanthin 38% (P < 0.001) concentrations increased after 5-wk of 1 egg/d compared with the phase prior to consuming eggs. Serum concentrations of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides were not affected. These findings indicate that in older adults, 5 wk of consuming 1 egg/d significantly increases serum lutein and zeaxanthin concentrations without elevating serum lipids and lipoprotein cholesterol concentrations.

Aged↗

PubMed2003

Quantification of carotenoids in chicken plasma after feeding free or esterified lutein and capsanthin using high-performance liquid chromatography and liquid chromatography-mass spectrometry analysis.

The present study reports about the plasma carotenoid levels of chickens achieved after feeding diets containing free and esterified lutein (from marigold) and capsanthin (from red pepper) by applying HPLC analyses using a RP-C30 column. Forty chickens were divided at random into four groups and were fed 2 wk with different diets after receiving a basal diet with a low carotenoid content for carotenoid depletion (3 wk). One group was fed a diet containing free lutein (G1), another group received a diet with esterified lutein (G2), two other diets contained free (R1) and esterified capsanthin (R2), respectively. To unequivocally identify plasma carotenoids, liquid chromatography-atmospheric pressure chemical ionization-mass spectrometry analysis was applied, which had never been used as an analytical tool to evaluate the carotenoids of chicken plasma; HPLC chromatograms of chicken plasma following capsanthin feeding have not been presented. The study showed that not only lutein but also capsanthin appeared in the blood stream after feeding free or esterified xanthophylls, demonstrating that capsanthin esters were bioavailable. Quantitative analysis showed comparable concentrations of plasma lutein and capsanthin, respectively, no matter if free or esterified carotenoids were fed.

Animal Nutritional Physiological Phenomena↗

PubMed1989

Effects of luteinizing hormone on superovulatory and steroidogenic responses of rat ovaries to infusion with follicle-stimulating hormone.

Immature female rats were infused s.c. continuously over a 60-h period with a partially purified porcine pituitary follicle-stimulating hormone (FSH) preparation having FSH activity 4.2 x NIH-FSH-S1 and luteinizing hormone (LH) activity 0.022 x NIH-LH-S1. High rates of superovulation were observed in rats receiving 1 U FSH/day, with 69 +/- 11 oocytes/rat recovered as cumulus-enclosed oocytes from oviducts on Day 1 (equivalent to the day of estrus). Addition of LH to the FSH, at dosages equivalent to 2.5-100 micrograms/day NIH-LH-S1 equivalents (2.5-100 mU) resulted in a dose-related inhibition of superovulation, reaching a nadir of 15 +/- 7 oocytes recovered from rats receiving 50 mU LH/day together with 1 U FSH/day. At the two highest LH doses, 50 and 100 mU/day, ovulation was advanced so that 12 +/- 3 and 15 +/- 4 oocytes, respectively, were recovered from oviducts of these rats flushed on the morning of Day 0, compared to none in rats infused with FSH alone. Ovarian steroid concentrations (ng/mg) observed on the morning of Day 0 in rats infused with FSH alone were progesterone, 0.50 +/- 0.13; testosterone, 0.16 +/- 0.08; androstenedione, 0.06; and estradiol, 0.23 +/- 0.05. On the morning of Day 1, ovarian progesterone concentrations in rats infused with FSH alone had risen to 3.30 +/- 0.33 ng/mg, whereas concentrations of testosterone, androstenedione, and estradiol, had fallen to essentially undetectable levels. Addition of LH to the FSH infusion resulted in dose-related increases, on Day 0, of all four steroids up to a dosage of 25 mU LH/day. At higher LH dosages, Day 0 ovarian concentrations of androgens and estradiol fell markedly, while progesterone concentrations continued to increase. Histological examination of ovaries revealed increases in the extent of luteinization of granulosa cells in follicles with retained oocytes on both Days 0 and 1 in rats infused with 25 and 50 mU LH/day together with 1 U FSH/day, compared to those observed in rats receiving FSH alone. These findings indicate that the elevated progesterone levels on Day 0 and inhibition of ovulation observed at these LH doses were due to premature luteinization of follicles, thus preventing ovulation. At lower LH doses, no sign (based on histologic or steroidogenic criteria) of premature luteinization was evident, suggesting that the decreased superovulation in these rats was due to decreased follicular maturation and/or increased atresia rather than to luteinization of follicles without ovulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1969

Luteinizing hormone-releasing activity in hypophysial stalk blood and elevation by dopamine.

Pituitary halves incubated in pituitary stalk plasma release more luteinizing hormone than their opposite halves incubated in plasma from peripheral blood. Glands incubated in stalk plasma from dopamine-treated rats release more luteinizing hormone than glands incubated in stalk plasma from untreated controls. Luteinizing hormone-releasing activity in stalk plasma may be due to the luteinizing hormone-releasing factor, and the secretion of luteinizing hormone-releasing factor may be controlled by a dopaminergic mechanism.

Animals↗

PubMed1972

Synthetic polypeptide antagonists of the hypothalamic luteinizing hormone releasing factor.

Two analogs of the hypothalamic luteinizing hormone releasing factor modified at the histidine-2 position were tested for biological activity (secretion of luteinizing hormone) in cultures of dispersed rat anterior pituitary cells. The analog in which glycine was substituted for histidine at position 2, [Gly(2)]LRF, behaves as a partial agonist releasing less than 50 percent of the luteinizing hormone secreted at maximum concentrations of the releasing factor, while the analog in which histidine at position 2 is deleted has no significant agonist activity at any of the doses tested. When added to the cultured cells at molar ratios 10(3) to 10(4) times that of the luteinizing hormone releasing factor, both analogs decrease the amount of luteinizing hormone secreted in response to the releasing factor.

Animals↗

PubMed1980

Progesterone administration in vivo stimulates release of luteinizing hormone-releasing hormone in vitro.

The release of luteinizing hormone-releasing hormone (LHRH) from tissue from the mediobasal hypothalamic-anterior hypothalamic-preoptic area of prepuberal female rats was measured in a perfusion system. Measurements were also made of the concentrations of LHRH in these tissue fragments and of luteinizing hormone in serum obtained when the rats were killed. Four groups of immature rats were studied: intact, ovariectomized, ovariectomized and implanted with estradiol-containing capsules, and ovariectomized rats primed with estradiol and injected with progesterone. The release of LHRH from the tissue of ovariectomized animals was significantly less than that of intact females and was not modified when the ovariectomized rats received estradiol. However, there was a four- to fivefold increase in LHRH release from tissue of ovariectomized rats primed with estradiol when they were killed 6 hours after they received an injection of progesterone. The concentrations of LHRH in tissue and of luteinizing hormone in serum varied among groups and with the time of day that the animals were killed. The interactions among luteinizing hormone, gonadal steroids, and the photoperiod seem to set the appropriate conditions for neural processes triggering a complete and normal release of luteinizing hormone.

Animals↗

PubMed2003

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

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

Age Factors↗

PubMed2001

A regulator of G protein signaling, RGS3, inhibits gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) secretion.

BACKGROUND: Luteinizing hormone secreted by the anterior pituitary gland regulates gonadal function. Luteinizing hormone secretion is regulated both by alterations in gonadotrope responsiveness to hypothalamic gonadotropin releasing hormone and by alterations in gonadotropin releasing hormone secretion. The mechanisms that determine gonadotrope responsiveness are unknown but may involve regulators of G protein signaling (RGSs). These proteins act by antagonizing or abbreviating interaction of Galpha proteins with effectors such as phospholipase Cbeta. Previously, we reported that gonadotropin releasing hormone-stimulated second messenger inositol trisphosphate production was inhibited when RGS3 and gonadotropin releasing hormone receptor cDNAs were co-transfected into the COS cell line. Here, we present evidence for RGS3 inhibition of gonadotropin releasing hormone-induced luteinizing hormone secretion from cultured rat pituitary cells. RESULTS: A truncated version of RGS3 (RGS3T = RGS3 314-519) inhibited gonadotropin releasing hormone-stimulated inositol trisphosphate production more potently than did RSG3 in gonadotropin releasing hormone receptor-bearing COS cells. An RSG3/glutathione-S-transferase fusion protein bound more 35S-Gqalpha than any other member of the G protein family tested. Adenoviral-mediated RGS3 gene transfer in pituitary gonadotropes inhibited gonadotropin releasing hormone-stimulated luteinizing hormone secretion in a dose-related fashion. Adeno-RGS3 also inhibited gonadotropin releasing hormone stimulated 3H-inositol phosphate accumulation, consistent with a molecular site of action at the Gqalpha protein. CONCLUSIONS: RGS3 inhibits gonadotropin releasing hormone-stimulated second messenger production (inositol trisphosphate) as well as luteinizing hormone secretion from rat pituitary gonadotropes apparently by binding and suppressing the transduction properties of Gqalpha protein function. A version of RGS3 that is amino-terminally truncated is even more potent than intact RGS3 at inhibiting gonadotropin releasing hormone-stimulated inositol trisphosphate production.

Animals↗

PubMed2005

Plasma appearance of labeled beta-carotene, lutein, and retinol in humans after consumption of isotopically labeled kale.

The bioavailability of carotenoids from kale was investigated by labeling nutrients in kale with 13C, feeding the kale to seven adult volunteers, and analyzing serial plasma samples for labeled lutein, beta-carotene, and retinol. Ingested doses of labeled carotenoids were 34 micromol for beta-carotene and 33 micromol for lutein. Peak plasma concentrations, areas under the plasma concentration-time curves (AUCs), and percentages of dose recovered at peak plasma concentrations were calculated. Average peak plasma concentrations were 0.38, 0.068, and 0.079 microM for [13C]lutein, [13C]beta-carotene, and [13C]retinol, respectively. Average AUC values (over 28 days) were 42.8, 13.6, 13.2 microM h for [13C]lutein, [13C]beta-carotene, and [13C]retinol, respectively. Percentages of dose recovered at peak plasma concentrations were 3.6, 0.7, and 0.7% for [13C]lutein, [13C]beta-carotene, and [13C]retinol, respectively. A positive relationship was observed between baseline plasma retinol levels and [13C]retinol plasma response. It is possible that this relationship was mediated either through some aspect of beta-carotene absorption or via the common pathways of metabolism for postdose and endogenous retinoid.

Adult↗

PubMed1976

Isolation and characterization of follicle-stimulating hormone and luteinizing hormone and its subunits from snapping turtle (Chelydra serpentina) pituitaries.

Highly purified luteinizing hormone and follicle-stimulating hormone have been isolated from extracts of snapping turtle (Chelydra serpentina) pituitaries. Both hormones are potent in non-mammalian gonadotropin bioassays (1.8 X NIH-LH-S1 and 30 X NIH-FSH-S1). The materials have been characterized by polyacrylamide gel electrophoresis, amino terminal group analysis, amino acid and carbohydrate content, and, in the case of turtle luteinizing hormone, ultracentrifugation. The luteinizing hormone was shown to dissociate and subunits were prepared by the countercurrent distribution technique and characterized. Biological activity of the hormone could be regenerated by recombination of the subunits. In addition, it was shown that the snapping turtle luteinizing hormone subunits could be combined with subunits from ovine luteinizing hormone with generation of significant biological activity. Comparisons in properties of the turtle gonadotropins have been made with ovine gonadotropins, showing, in many cases, similarities in properties, suggesting structural features which have been conserved during evolution.

Animals↗

PubMed1993

Hormone induction of luteinization and prostaglandin endoperoxide synthase-2 involves multiple cellular signaling pathways.

To determine the cellular signaling pathways involved in granulosa cell luteinization, known activators of protein kinase-A (LH and FSH) and protein kinase-C [GnRH and phorbol 12-myristate 13-acetate (PMA)] as well as inhibitors of tyrosine kinases (AG18 and genistein) were tested in an in vitro system using specific markers of luteinization (cell hypertrophy, side-chain cleavage cytochrome P450, and progesterone) and ovulation [prostaglandin endoperoxide synthase-2 (PGS-2)]. When preovulatory follicles were incubated in the presence of an ovulatory (500 ng/ml) dose of LH or high GnRH (1 microM), the granulosa cells harvested from these follicles assumed and maintained a stable luteal cell phenotype in vitro. Granulosa cells harvested from follicles incubated in subovulatory doses of LH (5 and 50 ng/ml), lower doses of GnRH (5, 50, and 500 nM), or PMA alone were unable to form a stable luteal cell phenotype. When PMA was combined with subovulatory doses of LH, granulosa cells luteinized, and PGS-2 protein was induced. AG18 (or genistein) blocked agonist induction of luteinization and of PGS-2 mRNA and protein when present during the first 2 h (0-2 h) of follicle incubation, but failed to block these events if added for the last 2 h (5-7 h of incubation). Combined, these results provide evidence to support a primary role for cAMP and protein kinase-A, a supportive but essential role for protein kinase-C, and an obligatory role for tyrosine kinases acting at an early stage in the cascade of events required for luteinization and ovulation.

Animals↗

PubMed1992

Administration of human luteinizing hormone (hLH) to macaques after follicular development: further titration of LH surge requirements for ovulatory changes in primate follicles.

After stimulation of multiple follicular development, endogenous LH surges elicited by GnRH or GnRH agonist were of insufficient duration (4-14 h) to evoke oocyte maturation and luteinization in this species. In this study, periovulatory LH surge requirements were further titrated using hLH as the ovulatory stimulus. Beginning at menses, rhesus monkeys were treated with human gonadotropins for 9 days to stimulate follicular growth. To induce ovulatory maturation on day 10, animals received: 1) hCG (1000 IU, im; n = 8); 2) highly-purified, urinary hLH (2542 IU, im; n = 4); or 3) hLH (2542 IU, im) followed by three injections of hLH (200 IU, im) at 8-h intervals (0800, 1600, 2400 h) daily during the luteal phase until menses (n = 3). Oocytes and luteinizing granulosa cells were obtained via follicle aspiration 27 h after the initial hLH or hCG injection. Estradiol and progesterone levels were measured in daily serum samples by RIA. Bioactive LH levels were determined at selected intervals within 36 h of the hLH ovulatory stimulus. Nuclear maturity of oocytes was evaluated as an indicator for reinitiation of meiosis. Luteinizing granulosa cells were processed for indirect immunocytochemistry using a monoclonal antibody to human progesterone receptor. In vitro progesterone production by luteinizing granulosa cells over 24 h was also assessed in the absence and presence of hCG. In all groups, serum estradiol rose to similar peak levels on day 10. After hLH, bioactive LH levels peaked (1262 +/- 79 ng/mL; mean +/- SEM) by 2-6 h, declined thereafter but remained above surge levels (100 ng/mL) for 18-24 h. Within 24 h of hLH injection, serum progesterone increased to 13 +/- 3 nmol/L, but returned to baseline in 1-6 days. In contrast, higher levels of progesterone were observed after hCG (114 +/- 51 nmol/L) and during luteal phase treatment with hLH (137 +/- 25 nmol/L) and the luteal phase was longer (11.5 +/- 0.4 and 14.3 +/- 0.7 days, respectively). Of the total cohort of oocytes aspirated, the proportion of oocytes resuming meiotic maturation (metaphase I plus metaphase II) was similar after hCG (76%) and hLH (74%). However, the proportion of oocytes maturing to metaphase II tended to be less (P = 0.08) after hLH (13%) than hCG (22%). Fertilization rates were similar between the two groups. Progesterone receptor was detected in nuclei of luteinizing granulosa cells from all animals receiving hCG, but only in some given hLH.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2006

Protective effect of lutein on ischemia-reperfusion injury in rat small intestine.

Lutein is a carotenoid and it has antioxidant effects. Lutein may have a protective effect on ischemia reperfusion (I/R) injury induced by free radical species. However, little is known about the protective effect of lutein on I/R injury in vivo. The present study was undertaken to clarify the protective effects of lutein on I/R injuries in the rat small intestine. Administration of lutein before intestinal I/R attenuated the damage to villi and deciduation of enterocytes and suppressed the increase in lipid peroxide.

Animals↗

PubMed1993

Biological activity of partially purified low molecular weight luteinizing hormone binding inhibitor in porcine follicular fluids.

We performed partial purification of low molecular weight luteinizing hormone binding inhibitor from porcine follicular fluids and examined its biological activities. Following ultrafiltration, gel filtration and anion exchange of the pooled porcine follicular fluids, low molecular weight fractions (500-10,000 MW) inhibited [125I]hLH binding to porcine granulosa cells in a dose-dependent manner. The binding inhibition kinetics study revealed that the luteinizing hormone binding inhibitor may indicate a non-competitive inhibition with [125I]hLH binding. In vitro bioassay using adult mouse testicular interstitial cells revealed that the partially purified luteinizing hormone binding inhibitor reduced ovine LH-stimulated testosterone and cAMP production in a dose-dependent manner, whereas the luteinizing hormone binding inhibitor did not affect basal production of testosterone and cAMP. The inhibitory activity was heat stable and did not disappear with activated charcoal adsorption. The results of the present study suggest that the luteinizing hormone binding inhibitor may play an important role as an ovarian non-steroidal regulator modulating the receptor binding of LH and LH-mediated steroidogenesis.

Animals↗