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At least 19 recordsLinked to original sources
PubMed1972

Luteinizing hormone receptors: specific binding of human luteinizing hormone to homogenates of luteinized rat ovaries.

Binding of human [(125)I]luteinizing hormone to homogenates of luteinized rat ovaries is dependent upon time, temperature, and pH and is saturable. Injection of human chorionic gonadotropin in vivo or addition of unlabeled human chorionic gonadotropin or human or ovine luteinizing hormone in vitro inhibits binding, whereas follicle stimulating hormone or prolactin is without effect. The dissociation constant for binding of luteinizing hormone receptor is 0.79 nM. The number of binding sites is 94 femtomol/mg of wet weight. NaCl, KCl, MgSO(4), and CaCl(2) at concentrations below 10 mM have no effect on binding, while all salts significantly inhibit binding at 150 mM. Binding of [(125)I]luteinizing hormone to its receptors is destroyed by proteolytic enzymes and by phospholipase C and D. The total binding activity is quantitatively recovered in the 2000 x g pellet of the homogenate.

Animals↗
PubMed1985

Simultaneous measurement of luteinizing hormone-releasing hormone and luteinizing hormone during estradiol-induced luteinizing hormone surges in the ovariectomized ewe.

Sequential bleeding and push-pull perfusion of the hypothalamus were used to characterize luteinizing hormone (LH) and LH-releasing hormone (LHRH) release in ovariectomized (OVX) ewes after injection of corn oil or estradiol benzoate (EB). Push-pull cannulae were surgically implanted into the stalk median eminences of 24 OVX ewes. Seven to 14 days later each of 20 animals was given an i.m. injection of 50 micrograms EB. Blood samples and push-pull perfusate were collected at 10-min intervals for 6-12 h beginning 12-15 h after EB injection. Four OVX ewes were given i.m. injections of corn oil 7 days after implantation of push-pull cannulae. Blood samples and push-pull perfusate were collected at 10-min intervals for 4 h between 18 and 22 h after injection of corn oil. Luteinizing hormone remained below 2 ng/ml throughout most of the sampling periods in 9 of 20 EB-treated ewes. In 5 of these 9 LHRH also was undetectable, whereas in 4 LHRH was detectable (1.84 +/- 0.29 pg/10 min), but did not increase with time. Preovulatory-like surges of LH occurred in 11 EB-treated ewes, but LHRH was undetectable in 5. In 4 of 6 ewes showing LH surges and detectable LHRH, sampling occurred during the onset of the LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Expression of receptors for luteinizing hormone-releasing hormone in human ovarian and endometrial cancers: frequency, autoregulation, and correlation with direct antiproliferative activity of luteinizing hormone-releasing hormone analogues.

OBJECTIVE: Several recent reports have demonstrated the expression of luteinizing hormone-releasing hormone receptors by human ovarian and endometrial cancers. Controversy persists on the relevance of this finding, in particular whether these receptors mediate direct antiproliferative effects of luteinizing hormone-releasing hormone analogues. We correlated the expression of luteinizing hormone-releasing hormone receptors by well-characterized ovarian and endometrial cancer cell lines with the ability of luteinizing hormone-releasing hormone analogues to reduce their proliferation and studied the autoregulation of luteinizing hormone-releasing hormone receptor expression by luteinizing hormone-releasing hormone agonist triptorelin and antagonist cetrorelix. The expression of luteinizing hormone-releasing hormone receptors was assessed in a series of specimens from primary ovarian and endometrial cancers. STUDY DESIGN: Luteinizing hormone-releasing hormone receptor expression was assessed by semiquantitative reverse transcriptase-polymerase chain reaction and radioligand binding assay. Antiproliferative effects were ascertained by proliferation assays in the absence or presence of luteinizing hormone-releasing hormone analogues. RESULTS: Ovarian (4/6 cell lines) and endometrial (5/6 cell lines) cancer cell lines expressed luteinizing hormone-releasing hormone receptors. The proliferation of these luteinizing hormone-releasing hormone receptor-positive cell lines was dose- and time-dependently reduced by agonistic and antagonistic luteinizing hormone-releasing hormone analogues. Luteinizing hormone-releasing hormone receptor density was reduced to 80% of controls (control, 100 %; P <.001) by luteinizing hormone-releasing hormone analogues. Seventy percent of primary ovarian cancers and 83% of primary endometrial cancers expressed luteinizing hormone-releasing hormone receptors. CONCLUSION: These findings suggest that luteinizing hormone-releasing hormone receptors that are expressed by human ovarian and endometrial cancer cell lines mediate direct antiproliferative effects of luteinizing hormone-releasing hormone analogues. Because most respective primary cancers expressed luteinizing hormone-releasing hormone receptors, these receptors might be used for novel antiproliferative therapeutic approaches and should be further evaluated.

Binding Sites↗
PubMed1992

Attenuated proestrous luteinizing hormone surges in middle-aged rats are associated with decreased pituitary luteinizing hormone-beta messenger ribonucleic acid expression.

OBJECTIVE: This study determined whether attenuated preovulatory luteinizing hormone surges in aging rats are associated with a decrease in pituitary luteinizing hormone content or luteinizing hormone beta-messenger ribonucleic acid expression on proestrus. STUDY DESIGN: Blood samples were taken every 90 minutes from 1:30 to 10:30 PM on proestrus in young (n = 8) and middle-aged (n = 12), regularly cyclic rats for plasma luteinizing hormone determination. On the next proestrus at 12 noon, rats were killed and the pituitaries were removed for luteinizing hormone content determination by radioimmunoassay and luteinizing hormone beta-messenger ribonucleic acid expression by dot blot analysis. Results were analyzed by one-way analysis of variance. RESULTS: Seven of the middle-aged rats had attenuated luteinizing hormone surges while the remaining five females had surges similar to those of young rats. On the next proestrus, all rats had similar quantities of pituitary luteinizing hormone. However, luteinizing hormone beta-messenger ribonucleic acid expression in middle-aged rats with attenuated luteinizing hormone surges was lower (p less than 0.05) than that of middle-aged and young rats with normal surges. CONCLUSION: Decreased luteinizing hormone beta-messenger ribonucleic acid expression, but not pituitary luteinizing hormone content at 12 noon on proestrus is correlated with attenuated luteinizing hormone surges in middle-aged rats.

Aging↗
PubMed1988

Luteinizing hormone-independent luteinization and ovulation in the hypophysectomized rat: a possible role for the oocyte?

Immature hypophysectomized, estrogen-treated rats were used to study the regulation of luteinization. Particular attention was focused on the potential role of the oocyte in this process. Rats were injected for 2 days with follicle-stimulating hormone (FSH) to stimulate follicular development. Within 48 h following FSH treatment, many follicles became luteinized, as determined by morphometric analysis. This luteinization occurred in the absence of detectable levels of luteinizing hormone (LH). The number of follicles undergoing luteinization was dependent on the FSH dose. In addition, ovulation occurred in some of the animals receiving the highest doses of FSH (3-micrograms or 5-micrograms injections). The majority of follicles undergoing luteinization or ovulation were greater than 400 microns in diameter. Luteinized follicles exhibited positive reactivity for cholesterol side-chain cleavage enzyme, 3 beta-hydroxysteroid dehydrogenase, lipid, and alkaline phosphatase, which was similar to that found in corpora lutea of the cycle. Serum progesterone (P0) and 20 alpha-hydroxypregn-4-en-one levels were elevated in animals with luteinized follicles, especially in those animals that also underwent ovulation. Morphological evaluation of oocytes showed that the majority of luteinized follicles contained a degenerating oocyte. Oocyte degeneration was highly correlated (r = 0.94) to luteinization. These results demonstrate that luteinization and ovulation can occur in the FSH/estrogen-primed hypophysectomized rats in the absence of detectable serum LH. Furthermore, LH-independent luteinization was strongly correlated to degenerative changes in the oocyte. These results provide new evidence to support the concept that the oocyte may be an intraovarian regulator of luteinization.

Animals↗
PubMed1986

Luteinizing hormone response to pulsatile luteinizing hormone-releasing hormone in prepubertal heifers.

The effects of 12 hourly 5-micrograms injections of luteinizing hormone-releasing hormone on luteinizing hormone release, were examined in 18 prepubertal Holstein heifers at 4, 7, or 10 mo of age. During a 6-h pretreatment period, mean serum luteinizing hormone concentrations and mean number of endogenous luteinizing hormone episodes per hour were not influenced by age. The 12-h treatment regimen induced a pulsatile release of luteinizing hormone in all heifers. The magnitude, pattern, and total amount of luteinizing hormone released were not influenced by age. However, in the 4 and 10-mo-old age groups, magnitude of luteinizing hormone response to the 3rd hourly injection of luteinizing hormone-releasing hormone was greater than the response to the second injection. Magnitudes of luteinizing hormone responses decreased with time after the 4th hourly injection through the 12th injection and patterns of decline appeared similar among the three age groups. The pituitary of the prepubertal dairy heifer is able to respond to an hourly pulsatile administration of luteinizing hormone-releasing hormone and this treatment regimen appears to produce a self-priming effect on luteinizing hormone release.

Animals↗
PubMed1994

European collaborative study of luteinizing hormone assay: 1. Epitope specificity of luteinizing hormone monoclonal antibodies and surface mapping of pituitary and urinary luteinizing hormone.

This report describes the results of the first part of the collaborative study organized by a working group sponsored by the Community Bureau of Reference of the European Community Commission. The whole study was designed to understand the causes of discrepancy among LH immunoassay methods. In the parent work, we studied the characteristics of 55 monoclonal antibodies to LH which allowed us to establish a detailed map of the antigenic surface of the hormone. In the present report we used this information to interpret the discrepancy in LH concentrations assayed with 12 different methods in 300 sera from subjects with various clinical conditions. The 55 monoclonal antibodies provided by 11 commercial companies were tested in various experiments: the apparent affinity of the antibodies was, generally but not always, higher for LH presented by a second antibody coated to plastic than for LH directly coated to plastic; 26% of the antibodies recognized the alpha subunit, 26% the beta subunit and 48% reacted only with the holomolecule (anti-alpha beta); only 28% of the antibodies were strictly specific for LH. Criss-cross experiments allowed us to distinguish 13 antigenic regions on the surface of LH: 6 were located on the alpha subunit, 3 on the beta subunit and 4 on the holomolecule. The monoclonal antibodies to the alpha beta regions further separated into 12 clusters of reactivity. Accordingly, LH appeared to exhibit at least 21 epitopes. Comparison of the immunoreactivity of various LH preparations indicated that highly purified pituitary LH and immunoaffinity purified urinary LH reacted similarly with the monoclonal antibodies and strongly differed from crude urinary LH. These data indicated that the immunoreactivity of an LH preparation depends mainly upon the degree of purification and not that much upon the origin of the preparation. The epitope specificity of the monoclonal antibodies used in 11 commercially available LH assay kits was also determined: 10 kits used at least one anti-alpha beta monoclonal antibody associated with an anti-beta monoclonal antibody in 7 cases or another anti-alpha beta monoclonal antibody in 3 cases; one kit used an anti-alpha monoclonal antibody associated with an anti-beta monoclonal antibody. None of the kits were strictly identical with regards to the epitope specificity of the monoclonal antibodies used.

Antibodies, Monoclonal↗
PubMed1981

Culture sensitization and inhibition of luteinizing hormone responsive production of cyclic AMP in luteal cells by luteinizing hormone, prostaglandin F2 alpha and [D-Trp6]-luteinizing hormone releasing hormone.

Many cells are able to regulate their sensitivity to hormones. In order to investigate the mechanism(s) by which rat luteal cells regulate their sensitivity to LH, we have developed and characterized a cell culture model. Cultures of dispersed rat luteal cells were exposed to graded doses of bovine LH, an analogue of LH releasing hormone (LH-RH) ([D-Trp6]-LH-RH), and prostaglandin F2 alpha (PGF2 alpha) for 3 h. The media containing these hormones were then replaced with fresh hormone-free medium and the cells cultured for 24 h. In order to test the sensitivity of these cultures after 24 h, the medium was discarded and replaced by medium alone, or medium containing a standard dose of bovine LH for 1 h. The amount of cyclic AMP accumulated during this hour was used as an index of the sensitivity of the cells to LH. Control cultures became 'supersensitive' to LH with augmented production of cyclic AMP during culture but LH-receptor binding activity was not increased. During the first 2 h of culture, LH (100 ng/ml) increased accumulation of cyclic AMP by fourfold, but after 5 h of culture, stimulation of cyclic AMP accumulation by the same dose of LH was increased 32-fold, 299-fold at 13 h and 359-fold at 21 h of culture. The increase in LH-responsive accumulation of cyclic AMP with cultured was severely impaired by early exposure of cells to LH, LH-RH analogue or PGF2 alpha during the first 2 h of culture. Also, both LH-RH analogue and PGF2 alpha acutely inhibited LH-stimulated accumulation of cyclic AMP. Inhibition of culture-induced sensitization of LH responsiveness was not altered by the addition of 3-isobutyl-1-methylxanthine. Scatchard analysis of LH binding sites indicated that pretreatment of luteal cells with LH (or human chorionic gonadotrophin at an equivalent dose) reduced the number of free LH receptors when measured after 24 h of culture, but total receptor binding activity was not changed. However, a similar effect was not seen with cells treated with PGF2 alpha or LH-RH analogue. It is suggested that 'culture-induced' supersensitivity may represent either recovery of pre-isolation sensitivity or result from the loss of an endogenous factor(s) which retards the coupling of the LH receptor and adenylate cyclase. Although PGF2 alpha and LH-RH analogue have been shown to directly prevent the occupied LH receptor from activation of adenylate cyclase, the present observations have indicated that this inhibitory process was continued even when these agents were removed from the culture medium.

Animals↗
PubMed1998

Lutein ester in serum after lutein supplementation in human subjects.

Lutein, one of the major carotenoids present in serum, is also widely consumed by most populations. For the purpose of testing the potential health benefits of several carotenoids, lutein was supplied as part of an intervention trial to test whether the consumption of these food constituents reduces oxidative damage to human tissue components. Lutein from a natural source (15 mg/d as mixed ester forms) was supplied for 4 months to eighteen non-smoking, apparently healthy volunteers (nine men, nine women) aged 25-45 years. The serum carotenoid profile was analysed at baseline and monthly thereafter. On average, lutein concentrations increased 5-fold after the first month of supplementation (mean 1.34 (range 0.6-3.34) mumol/l). On reviewing the results, in those volunteers whose lutein levels surpassed 1.05 mumol/l (fourteen of seventeen), we tentatively identified lutein monopalmitate along with another unidentified ester (possibly from a monoketocarotenoid) in serum. Lutein levels returned to baseline values and ester forms were not present 3 months after supplementation was discontinued. Their concentrations did not correlate with, and represented less than 3% of, lutein levels achieved in serum. They were observed before development of, and despite the presence of, carotenodermia. To our knowledge, this is the first time xanthophyll esters have been described in human serum. In view of the fact that xanthophyll esters have not been previously reported in serum and chylomicrons, it seems unlikely that these ester forms would be a reflection of the contents of the capsule. They may indicate a 'ceiling effect' on or saturation of the transport capacity for xanthophylls, and may have been re-esterified in vivo because of the unusual dietary conditions. The determination of the physiological importance of this finding will require further investigation, although neither haematological nor biochemical changes were detected.

Adult↗
PubMed1993

Premature luteinization is not eliminated by pituitary desensitization with leuprolide acetate in women undergoing gonadotrophin stimulation who demonstrated premature luteinization in a prior gonadotrophin-only cycle.

A total of 40 women who demonstrated premature luteinization (serum progesterone > or = 3.5 nmol/l (1.1 ng/ml) on or before the day of human chorionic gonadotrophin (HCG) administration) during ovarian stimulation with human menopausal gonadotrophins (HMG) were restimulated in 46 subsequent cycles after pituitary desensitization with the gonadotrophin-releasing hormone agonist (GnRHa, 1 mg), leuprolide acetate. Five women were treated with a double dose of agonist (2 mg) when premature luteinization was determined on the single dose protocol. In HMG-only cycles, a frank luteinizing hormone (LH) surge was detected in 30 cycles; 15 cycles were cancelled because of premature ovulation. In agonist cycles there were no cancellations, although 25 cycles demonstrated premature luteinization and in six cycles a frank LH surge was detected. Doubling the dose of the agonist did not prevent premature luteinization. Agonist cycles with and without premature luteinization did not differ in any in-vitro fertilization (IVF) outcome parameters (ampoules of gonadotrophins, day of HCG administration, peak oestradiol concentration, number of oocytes retrieved, fertilized, transferred or cryopreserved). We conclude that in patients who demonstrate premature luteinization in a gonadotrophin-only cycle, pituitary desensitization may not completely eliminate subtle luteinization or a frank LH surge.

Chorionic Gonadotropin↗
PubMed2002

Differentiation between lutein monoester regioisomers and detection of lutein diesters from marigold flowers (Tagetes erecta L.) and several fruits by liquid chromatography-mass spectrometry.

Liquid chromatography-atmospheric pressure chemical ionization mass spectrometry (LC-APCIMS) was employed for the identification of eight lutein monoesters, formed by incomplete enzymatic saponification of lutein diesters of marigold (Tagetes erecta L.) by Candida rugosa lipase. Additionally, the main lutein diesters naturally occurring in marigold oleoresin were chromatographically separated and identified. The LC-MS method allows for characterization of lutein diesters occurring as minor components in several fruits; this was demonstrated by analysis of extracts of cape gooseberry (Physalis peruviana L.), kiwano (Cucumis metuliferus E. Mey. ex Naud.), and pumpkin (Cucurbita pepo L.). The assignment of the regioisomers of lutein monoesters is based on the characteristic fragmentation pattern: the most intense daughter ion generally results from the loss of the substituent (fatty acid or hydroxyl group) bound to the epsilon-ionone ring, yielding an allylic cation. The limit of detection was estimated at 0.5 microg/mL with lutein dimyristate as reference compound. This method provides a useful tool to obtain further insight into the biochemical reactions leading to lutein ester formation in plants.

Asteraceae↗
PubMed1988

Dose-related inhibition of acute luteinizing hormone response during luteinizing hormone-releasing hormone agonist treatment for uterine leiomyoma.

Twenty-six women with uterine leiomyoma were treated for 6 months with subcutaneous injections of the luteinizing hormone-releasing hormone agonist buserelin. Eight women received 200 micrograms daily, eight women received 350 micrograms daily, and 10 women after initial administration of 200 micrograms every 8 hours for 7 days, 500 micrograms of buserelin was administered daily. After 1, 3, and 6 months of treatment, serum luteinizing hormone levels were measured before and 4 and 8 hours after the administration of buserelin. The area under the curve for acute luteinizing-hormone response was then individually calculated. The inhibition of acute luteinizing hormone response during luteinizing hormone-releasing hormone agonist treatment was proportional to the dosage used and remained constant during the treatment period.

Adult↗
PubMed1988

Effect of preovulatory estradiol concentrations on luteinizing hormone diurnal secretory patterns: a hypothesis for the timing of the luteinizing hormone surge.

The effect of preovulatory estradiol concentrations on 24-hour patterns of luteinizing hormone secretion was studied in six women with normal menstrual cycles. Blood samples were collected every 15 minutes for 24 hours before and after 7 days of estradiol benzoate administration, which achieved mean (+/- SE) estradiol concentrations of 424 +/- 54 pg/ml. The luteinizing hormone pulse frequency decreased significantly during sleeping hours both before (p less than 0.05) and after (p less than 0.005) estradiol benzoate administration. After estradiol benzoate, there also was diurnal variation in overall mean luteinizing hormone concentrations, which markedly increased secretion in the morning hours. The diurnal changes in luteinizing hormone secretion varied inversely with those of prolactin. These findings are consonant with the observation that the onset of the preovulatory luteinizing hormone surge in women occurs most frequently in the early morning hours.

Adult↗
PubMed1990

Prolonged inhibition of luteinizing hormone and testosterone levels in male rats with the luteinizing hormone-releasing hormone antagonist SB-75.

Inhibitory effects of the potent antagonist of luteinizing hormone-releasing hormone N-Ac-[3-(2-naphthyl)-D-alanine1,4-chloro-D-phenylalanine2,3- (3-pyridyl)-D- alanine3,D-citrulline6,D-alanine10]luteinizing hormone-releasing hormone (SB-75) free of edematogenic effects were investigated in male rats. In a study to determine the effect on luteinizing hormone levels in castrated male rats, SB-75 was injected s.c. in doses of 0.625, 1.25, 2.5, 5.0, and 10 micrograms. Blood samples were taken at different intervals for 48 hr. All doses of SB-75 significantly decreased luteinizing hormone levels for greater than 6 hr (P less than 0.01); this inhibition lasted for greater than 24 hr (P less than 0.01) with a dose of 5.0 micrograms and greater than 48 hr with 10 micrograms (P less than 0.05). Serum testosterone levels were also measured in intact male rats injected with SB-75 in doses of 25, 50, and 100 micrograms. All doses produced a dramatic fall in testosterone to castration levels 6 hr after injection (P less than 0.01); this inhibition of serum testosterone was maintained for greater than 72 hr, but only the 100-micrograms dose could keep testosterone in the castration range for greater than 24 hr (P less than 0.01). In another study using a specific RIA, we obtained the pharmacokinetic release pattern of SB-75 from two sustained delivery formulations of SB-75 pamoate microgranules and examined their effect on serum testosterone. After a single i.m. injection of 20 mg of one batch of microgranules, a large peak corresponding to SB-75 at 45.8 ng/ml was observed, corresponding to the "burst" effect. Levels of the analog decreased to 19.6 ng/ml on day 2, gradually reached a concentration of 4.7 ng/ml on day 7, and kept declining thereafter. Testosterone levels were reduced on day 1 (P less than 0.01) and were maintained at low values for greater than 7 days (P less than 0.05). In rats injected with 10 mg of SB-75 pamoate microgranules of the second batch, SB-75 serum levels rose to 33 ng/ml 3 hr after administration and then fell gradually to approximately 3.4 ng/ml on day 16, but a second small peak was seen on day 28. Subsequently, the analog levels decreased slowly to 2.9 ng/ml on day 42. At this time, testosterone serum levels were still significantly lower than in controls. These overall results demonstrate the efficacy of SB-75 in the suppression of the pituitary-gonadal axis. This modern luteinizing hormone-releasing hormone antagonist can possibly be used for treating sex hormone-sensitive cancers and other disorders.

Animals↗