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PubMed1982

Response to luteinizing releasing hormone, thyrotrophic releasing hormone, and human chorionic gonadotropin administration in healthy men at different risks for prostatic cancer and in prostatic cancer patients.

A comparative study of the pituitary and testicular response to luteinizing releasing hormone (LHRH), thyrotrophic releasing hormone (TRH), and human chorionic gonadotrophin (HCG) administration was carried out in (a) low-risk young South African black men and high-risk North American black men for prostatic cancer and (b) healthy elderly South African men and South African black men with prostatic cancer. A comparable HCG response occurred in young South African and North American black men, while a greater release of prolactin, but a lesser release of luteinizing hormone in response to LHRH:TRH occurred in South African black men. The response to HCG was comparable in elderly and young South African black men, although the prolactin release in response to TRH was greater in elderly men. A more prolonged release of luteinizing hormone was evident in men with prostatic cancer. Higher estradiol and estrone but lower androstenedione levels occurred in men with prostatic cancer. Data suggest that, in the elderly South African black men with prostatic cancer, estrogen metabolism is modified and that either the estrogen level or the higher estrogen:androgen levels modify the pituitary response to LHRH:TRH. A Western diet enhanced the changes in hormone profiles evident in black South African men with prostatic cancer.

Adult↗

PubMed1982

Effects of ketamine-xylazine anesthesia on blood levels of luteinizing hormone and follicle stimulating hormone in rabbits.

The effect of injection of an anesthetic dose of ketamine (70mg/kg) followed by xylazine (5mg/kg) on blood levels of luteinizing hormone and follicle stimulating hormone was measured in female rabbits. The drug combination caused a measurable suppression of follicle stimulating hormone levels in both castrated does and during the postovulatory follicle stimulating hormone surge in mated rabbits. Blood luteinizing hormone was low in these two animal model systems and was not further suppressed by ketamine-xylazine injections. When mated rabbits were injected with the drugs immediately postcoitum, ovulation and the preovulatory surge of luteinizing hormone and follicle stimulating hormone failed to occur in two of six treated animals. The results of these studies showed that ketamine-xylazine injections suppressed certain episodes of gonadotropin release in the female rabbit. However, the suppression was transitory and without apparent permanent effect.

Anesthesia, General↗

PubMed1981

Cell-free synthesis and processing of the precursors to the subunits of luteinizing hormone.

Polyadenylated RNA prepared from pituitary glands of ovariectomized rats was translated in heterologous cell-free systems derived from wheat germ and rabbit reticulocytes in the absence and in the presence of pancreatic microsomal membranes. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated that the major 14,000-dalton product immunoprecipitated by antisera to the alpha subunit of rat and bovine luteinizing hormone from membrane-free translations was processed to a major 21,000-dalton and a minor 17,000-dalton product in the presence of microsomal membranes. These membrane-dependent products were sensitive to cleavage by the glycosidase endo-beta-N-acetylglucosaminidase H, but the 14,000-dalton product was resistant. The 21,000-dalton product was sequestered within the microsomal vesicles as shown by its resistance to limited proteolysis capable of digesting the 14,000-dalton precursor. Glycosylated products with apparent Mr = 18,000 and 17,000 were identified from membrane-supplemented translations by immunoprecipitation using antisera to the beta subunit of rat luteinizing hormone. The immunological identity of the glycosylated subunits of luteinizing hormone was confirmed by showing competition of the immunoprecipitation reactions with unlabeled subunits.

Animals↗

PubMed1993

[The character of the interaction of beta-carotene-15,15'-dioxygenase from rabbit small intestine with lycopene, 15,15'-dehydro-beta-carotene, lutein, and astaxanthine].

Interaction of rabbit small intestine mucosa beta-carotene 15,15'-dioxygenase with lycopene, 15,15'-dehydro-beta-carotene, lutein and astaxanthine is unaccompanied by the formation of products of enzymatic cleavage of the central double bond of these carotenoid molecules. Apo-carotenoids of lutein and lycopene are formed by nonenzymatic oxidation. Lycopene and 15,15'-dehydro-beta-carotene competitively inhibit the enzymatic oxidation of beta-carotene. Inhibition of the enzyme conversion by lutein and astaxanthin is less strong, being of a competitive-noncompetitive type. Enzymatic formation of retinal from beta-carotene depends on the accessibility of substrate molecules.

Animals↗

PubMedDate not supplied

Effect of beta-carotene, canthaxanthin, or lutein on lymphocyte proliferation (in vitro) of newly hatched chicks.

The aim of this study was to determine the effect of beta-carotene, canthaxanthin, and lutein on lymphocyte proliferation (in vitro) of newly hatched chicks. Tetrahydrofuran (THF) was used as the vehicle to introduce carotenoids in the culture media. So, we also determined effect of THF on viability of cells. The viabilities of fibroblast cells at 10(-3) dilution were 98% and 96% after 24 and 48 hr of incubation. Therefore, 10(-3) (v/v) THF dilution was decided upon as the vehicle to introduce carotenoids in culture media. Chick bursal lymphocytes were incubated in the presence or absence of beta-carotene, canthaxanthin, or lutein and stimulated with phorbol 12, 13-dibutyrate. The results of this experiment suggested that THF rather than the carotenoids stimulated bursal lymphocyte proliferation. The mechanism by which THF acted as a mitogen is not known. We conclude from this study that beta-carotene, canthaxanthin, and lutein are not effective in enhancing in vitro bursal lymphocyte proliferation at concentrations of less than 10(-6) M in the presence of THF.

Analysis of Variance↗

PubMedDate not supplied

[Gonadotropin from the bovine pineal body. Evidence of its similarity with the luteinizing hormone of the pituitary gland].

Gonadotropin affiliated by biological and immunochemical properties to the luteinizing hormone of the hypophysis was revealed in the purified extracts from the bovine pineal glands. Biological properties of gonadotropin from the pineal glands were assessed by the reactions specific of the luteinizing hormone. Immunochemical properties of gonadotropin were studied by means of gel-precipitation in agar gel, immunoelectrophoresis and radioimmunochemical analysis. It was found that the specific content of gonadotropin in the epiphysis was 80 times lower than the specific content of the luteinizing hormone in the hypophysis, but exceeded the LH concentration in the blood serum 555 times and in the cerebrospinal fluid 6.8 times. Immunoreactive LH was absent in the extracts of the brain cortex, the liver and the ovaries. A theoretical interpretation of a possible physiological role of the LH-like gonadotropin in the endocrine regulation of the reproductive function of the organism is given in this work.

Animals↗

PubMed1975

Action of luteinizing hormone-releasing factor (lrf) in the initiation of lordosis behavior in the estrone-primed ovariectomized female rat.

In order to evaluate the precise role of luteinizing hormone-releasing factor (LRF) in mediating the onset of sexual behavior, the specificity, time-course, and dose-response relationship of LRF-facilitated lordosis behavior were determined. Ovariectomized female rats, pretreated with estrone and LRF, displayed a pattern of lordosis behavior which differed little from that produced by estrone-progesterone. Little if any lordosis behavior was observed in response to LRF alone, estrone alone, or estrone in combination with luteinizing hormone (LH), follicle-stimulating hormone (FSH), or thyrotropin-releasing factor (TRF). Furthermore, LRF-induced lordosis behavior occurred in the absence of the adrenals, thus eliminating adrenal progesterone as a factor in facilitating the appearnce of lordosis behavior. The LRF-facilitated lordosis behavior was seen 2 h after the injection of LRF and was maintained for a total of 8 h. A minimal dose of 150 ng LRF was required to initiate the first consistent appearance of lordosis behavior; the maximum response was obtained with 500 ng. It is thus suggested that LRF is not only responsible for the ovulatory discharge of LH and subsequent ovulation, but may also play a role in the initiation of the onset of mating behavior in the female rat.

Adrenal Glands↗

PubMed2000

Early prenatal sonographic diagnosis of twin triploid gestation presenting with fetal hydrops and theca-lutein ovarian cysts.

The presence of theca-lutein ovarian cysts in the early second trimester of pregnancy is highly suspicious for a complete hydatidiform molar pregnancy but can be seen in association with a partial mole. Theca-lutein cysts may occur following hormonal stimulation for assisted reproductive techniques or in association with multiple gestations. Rare causes include immune and nonimmune fetal hydrops, maternal hypothyroidism, and triploid gestations. We report a case of a monochorionic twin gestation in which prenatal sonography demonstrated multiple anomalies and hydrops in each twin and bilateral theca-lutein ovarian cysts. Triploidy in both twins and a partial hydatidiform mole were confirmed at pathologic examination.

Abnormalities, Multiple↗

PubMed1998

Regulation of follicular luteinization by a gonadotropin-releasing hormone agonist: relationship between steroidogenesis and apoptosis.

The purpose of this study was to evaluate the effects of GnRH-analog (Leuprolide acetate, LA) administration on follicular luteinization in equine chorionic gonadotropin plus human chorionic gonadotropin (eCG + hCG)-superovulated prepubertal treated rats. Results indicate that LA treatment decreases circulating levels of progesterone (P) and P accumulation in collagenase-dispersed ovarian cell cultures, though estradiol (E2) production is increased. These data suggest that cells from the LA group may be less luteinized following gonadotropin treatment. Studies performed on histological ovarian sections after different times of eCG administration showed that LA injections produce lower amounts of corpora lutea and antral follicles, and a greater number of atretic and preantral follicles. The basal and LH-stimulated P and progestagen accumulations are decreased in incubations of corpora lutea isolated from the LA group. In addition, the mitochondrial cholesterol side-chain cleavage (P450SCC) levels in corpora lutea from LA-treated rats are reduced, indicating that the decrease in P production observed is due in part to an alteration in the steroidogenic luteal capability. Immunocytochemical localization of nuclei exhibiting DNA fragmentation by the technique of terminal deoxynucleotidyl transferase end-labeling showed that LA treatment causes an increase in the number of apoptotic cells in preantral and antral follicles at all times studied (1, 2, 4, or 7 days of LA administration). A similar effect, though less pronounced, was observed in corpora lutea. It is concluded that LA treatment produces a failure in the steroidogenic luteal capability and an increase of apoptotic mechanisms in the ovary, producing as a consequence an interference in the follicular recruitment, growth, and luteinization induced by gonadotropins.

Animals↗

PubMed1979

Structural biochemistry XIII: Synthesis of luteinizing hormone-releasing hormone modification [Trp8]-LH-RH.

A fragment condensation method was utilized for synthesis of the Trp8-substituted luteinizing hormone-releasing hormone (LH-RH). tert-Butoxycarbonyl protection was employed for the alpha-amino positions, and benzyl protection was used for the phenol group of Tyr and the imidazole nitrogen of His. Peptide bond-forming reactions were performed using N-hydroxysuccinimide (for Trp), dicyclohexylcarbodiimide-1-hydroxybenzotriazole, 1-ethyl-3-(3'-dimethylaminopropyl)-carbodiimide hydrochloride, or mixed carbonic anhydride methods. Biological evaluation of [Trp8]-LH-RH indicated no luteinizing hormone-releasing activity or inhibition of luteinizing hormone release over the dose ranges studied.

Animals↗

PubMed2006

hCG-dependent regulation of angiogenic factors in human granulosa lutein cells.

As prerequisite for development and maintenance of many diseases angiogenesis is of particular interest in medicine. Pathologic angiogenesis takes place in chronic arthritis, collagen diseases, arteriosclerosis, retinopathy associated with diabetes, and particularly in cancers. However, angiogenesis as a physiological process regularly occurs in the ovary. After ovulation the corpus luteum is formed by rapid vascularization of initially avascular granulosa lutein cell tissue. This process is regulated by gonadotropic hormones. In order to gain further insights in the regulatory mechanisms of angiogenesis in the ovary, we investigated these mechanisms in cell culture of human granulosa lutein cells. In particular, we determined the expression and production of several angiogenic factors including tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), Leptin, connective tissue growth factor (CTGF), meningioma-associated complimentary DNA (Mac25), basic fibroblast growth factor (bFGF), and Midkine. In addition, we showed that human chorionic gonadotropin (hCG) has distinct effects on their expression and production. hCG enhances the expression and production of TIMP-1, whereas it downregulates the expression of CTGF and Mac25. Furthermore it decreases the expression of Leptin. Our results provide evidence that hCG determines growth and development of the corpus luteum by mediating angiogenic pathways in human granulosa lutein cells. Hence we describe a further approach to understand the regulation of angiogenesis in the ovary.

Angiogenesis Inducing Agents↗

PubMed1999

Induction of apoptosis in luteinized granulosa cells by the MAP kinase kinase (MEK) inhibitor PD98059.

Our objective is to test the hypothesis that inhibition of mitogen-activated protein (MAP) kinase kinase (MEK) with PD98059 in human luteinized granulosa cells will block epidermal growth (EGF)-stimulated MAP kinase activity and induce apoptosis. Luteinized granulosa cells from human in vitro fertilization aspirates were cultured and treated with the following: (1) vehicle; (2) PD98059; (3) EGF; (4) PD98059 + EGF. Treatment with PD98059 suppressed MAP kinase activity, inhibited MAP kinase phosphorylation by Western blot analysis, blocked nuclear translocation of phosphorylated MAP kinase by confocal microscopy, and increased percentages of subdiploid apoptotic nuclei by flow cytometry. Our data are the first evidence that a relationship may exist between the MAP kinase pathway and control of apoptosis in human luteinized granulosa cells. These results support the hypothesis that suppression of the MAP kinase pathway may lead to apoptosis in these cells.

Apoptosis↗

PubMed2000

NPC1-containing compartment of human granulosa-lutein cells: a role in the intracellular trafficking of cholesterol supporting steroidogenesis.

Steroidogenic cells represent unique systems for the exploration of intracellular cholesterol trafficking. We employed cytochemical and biochemical methods to explore the expression, regulation, and function of the Niemann-Pick C1 protein (NPC1) in human granulosa-lutein cells. NPC1 was localized in a subset of lysosome-associated membrane glycoprotein 2 (LAMP-2)-positive vesicles. By analyzing the sensitivity of NPC1 N-linked oligosaccharide chains to glycosidases and neuraminidase, evidence was obtained for movement of nascent NPC1 from the endoplasmic reticulum through the medial and trans compartments of the Golgi apparatus prior to its appearance in cytoplasmic vesicles. NPC1 protein content and the morphology and cellular distribution of NPC1-containing vesicles were not affected by treatment of the granulosa-lutein cells with 8-Br-cAMP, which stimulates cholesterol metabolism into progesterone. In contrast, steroidogenic acute regulatory (StAR) protein levels were increased by 8-Br-cAMP. Incubation of granulosa-lutein cells with low-density lipoprotein (LDL) in the presence of the hydrophobic amine, U18666A, caused accumulation of free cholesterol in granules, identified by filipin staining, that contained LAMP-2 and NPC1. These granules also stained for neutral lipid with Nile red, reflecting accumulation of LDL-derived cholesterol esters. LDL-stimulated progesterone synthesis was completely blocked by U18666A, leaving steroid output at levels similar to those of cells incubated in the absence of LDL. The hydrophobic amine also blocked the LDL augmentation of 8-Br-cAMP-stimulated progesterone synthesis, reducing steroid production to levels seen in cells stimulated with 8-Br-cAMP in the absence of LDL. Steroidogenesis recovered after U18666A was removed from the culture medium. U18666A treatment caused a 2-fold or more increase in NPC1 protein and mRNA levels, suggesting that disruption of NPC1's function activates a compensatory mechanism resulting in increased NPC1 synthesis. We conclude that the NPC1 compartment plays an important role in the trafficking of LDL-derived substrate in steroidogenic cells; that NPC1 expression is up-regulated when NPC1 action is blocked; and that the NPC1 compartment can be functionally separated from other intracellular pathways contributing substrate for steroidogenesis.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2000

Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer.

OBJECTIVES: The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesions-ovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression in OET was also examined. METHODS: Fifteen microdissected samples of ovarian surface epithelium (OSE), 20 OEIs from benign ovaries, and 141 OETs, including 48 cystadenomas, 33 borderline tumors, 60 carcinomas, and 5 metastatic cancers, were examined for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. RESULTS: LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27% of cases and in the stromal compartment in 37% of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42% of benign, 24% of borderline, and 17% of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic to the ovary. LHR transcription splicing variants from a single previous report were confirmed in this study. CONCLUSIONS: Malignant OETs have significant reduction of LHR expression compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone in serum may have direct influence on tumor growth, whereas the receptor in tumor stroma may be indicative of a paracrine function of LH in the development of OETs.

Adolescent↗

PubMed1975

Ultrastructural changes in granulosa lutein cells and progesterone levels during preimplantation, implatation, and early placentation in the western spotted skunk.

The ultrastructure of corpora lutea obtained during the preimplantation implantation and early post-implantation periods has been studied in 20 western spotted skunks. Fine structure of granulosa lutein cells was correlated with progesterone levels. The corpus luteum of the prolonged (7 month) preimplantaion period contained undifferentiated small granulosa cells and differentiated large granulosa lutein cells. The former ranged in size between 12 and 20 mu and the latter between 20 and 45 mu. The ratio of small and large cells was about equal in an animal 2 days prior to nidation whereas only few small cells and numerous large cells were observed in an animal estimated to be 8 to 12 hours from nidation. Occasionally small cells were observed amidst large ones during the 24 hour nidation period, i.e. adhesion of trophoblast with the luminal uterine epithelium, but small cells were absent in animals after this period. Small cells had some smooth and rough endoplasmic reticulum rod-shaped mitochondria with plate-like cristae, small Golgi complex, and relatively smooth plasma membranes. Large lutein cells had abundant smooth endoplasmic reticulum, membranous whorls of smooth endoplasmic reticulum, usually round mitochondria with tubular and lamellar cristae, a well developed Golgi complex, variable amounts of lipid droplets, and highly plicated and ruffled plasma membranes. Peripheral plasma progesterone levels during the prolonged preimplantation period ranged between 1.1 and 7.9 ng/ml, but during implantation it was between 8 and 16.6 ng/ml. It is suggested that plasma progesterone levels fluctuate during the time of implantation and should not be regarded as a basis to predict actual nidation in the western spotted skunk.

Animals↗

PubMed1990

Luteinization of human granulosa cells in vivo is associated with expression of MHC class II antigens.

We previously described the presence of MHC class II (HLA-DR) antigens, structurally similar to those on lymphoid cells and bearing the genetically-appropriate allotypic determinants, on human adrenocortical cells in the zona reticularis of normal glands. We now report a similar expression by granulosa-lutein cells (GLC) in corpora lutea (CL) of normal ovaries, as detected by indirect immunofluorescence techniques with the use of mouse monoclonal antibodies (MAb). In some cases, GLC were also positive for HLA-DQ and -DP antigen expression. Neither granulosa nor theca interna cells in large antral follicles of the same ovaries showed any detectable expression of MHC class II antigens. Moreover, theca-lutein (paralutein) cells, identified by their reactivity with specific human autoantibodies in 5 of the 7 human CL examined, were also negative. Similarly, GLC, but not paralutein cells, in rhesus monkey CL showed significant cross-reactivity with anti-HLA-DR MAb. In contrast, lutein cells in ovaries from either cycling or 7-day-pregnant rats were negative for MHC class II (Ia) antigen expression. Expression of MHC class II antigens by human granulosa cells after their luteal transformation confirms the normal inducibility of certain human steroidogenic cells at the time of their further functional differentiation and enhanced biosynthetic activity, and suggests that these molecules may have additional functions beyond serving as restriction elements in the immune response.

Adult↗

PubMed1990

Immunocytochemical localization of oxytocin in corpora lutea and luteinized cysts from anoestrous ewes stimulated with gonadotrophin-releasing hormone.

Anoestrous Romney Marsh ewes with or without progesterone pretreatment were injected with multiple low-doses of gonadotrophin-releasing hormone followed by a single, larger bolus. Blood samples were taken at twelve-hourly intervals for progesterone radioimmunoassay. Ewes were slaughtered on day 3 or 5 after the bolus injection, and the ovaries were collected for histology and immunocytochemical examination for oxytocin-immunoreactivity. The corpora lutea of all ewes killed on day 3 had similar weights and morphology. The ovaries of those ewes which were not pretreated with progesterone also contained some luteinized cysts. Ewes slaughtered on day 5 were separated into 2 groups according to plasma progesterone profiles, which were either rising ('normal'), or falling after a transitory rise ('abnormal'). Those ewes pretreated with progesterone all had a 'normal' progesterone profile whereas, of 14 ewes not pretreated with progesterone, 6 were 'normal' and 8 'abnormal'. Corpora lutea were significantly lighter in the 'abnormal' group and the ovaries of most of these ewes also contained luteinized cysts. All corpora lutea and luteinized cysts showed staining for oxytocin-immunoreactivity although the staining intensity was variable. In corpora lutea from 'normal' ewes oxytocin was restricted to large luteal cells. In addition tissues from 'abnormal' ewes also contained many cells with an atypical elongated shape which stained for oxytocin-immunoreactivity. These results show that progesterone pretreatment is needed for both normal morphological and endocrine development of corpora lutea in anoestrous ewes stimulated with gonadotrophin-releasing hormone.

Anestrus↗

PubMed1991

Fibrocystic disease of the breast in premenopausal women: histohormonal correlation and response to luteinizing hormone releasing hormone analog treatment.

Sixty-six patients with fibrocystic mastopathy were enrolled in the trial after being selected according to clinical, radioultrasonographic, and histologic criteria. No characteristic hormonal profile was noted in most patients (52%). Estrogen receptors or progesterone receptors, or both, were found in 57% of patients. Hormone receptor levels were correlated with atypical proliferative mastopathy (87.5%). Mastopathy was associated with a uterine fibroma or a fibromatous uterus in 73% of cases. All patients received intramuscular injections of a sustained delivery system (microcapsules) of luteinizing hormone releasing hormone agonist [D-Trp6]-LHRH, Ipsen-Biotech, Paris) for 3 to 6 months. In case of partial response at 3 months, an antiestrogen (tamoxifen, 40 mg/day, for estrogen receptor-predominant lesions) or a progestin (cyproterone acetate, 50 mg/day, for progesterone receptor-predominant lesions) was added to the luteinizing hormone releasing hormone agonist. A complete response was observed in more than half of the patients (n = 35, 53%) treated by [D-Trp6]-LHRH alone (n = 29) or associated with tamoxifen (n = 4) or cyproterone acetate (n = 2). A significant partial response was observed in 30 other patients (45%). Additionally, half of them received inhibitory drugs. The best responses were seen with cyst reformation (complete response, 100%) and fibrous block. Clinical responses to treatment with [D-Trp6]-LHRH alone were independent of hormone receptor status, but synergistic effects occurred with concomitant use of the corresponding inhibitory drugs. We conclude that chronic mastopathy, particularly when associated with uterine fibroma, can be successfully treated by luteinizing hormone releasing hormone analogs in premenopausal women.

Adult↗