Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted on male Wistar rats. A study was made of the intensity of incorporation into the liver, kidneys, the thyroid gland, the adrenal glands and the rate of elimination from the blood plasma of two ACTH preparations iodated by Greenwood's method: International Standard for Corticotropin, Mill Hill, London; Hum ACTH--Hid-28, Richter. It appeared that the preparations of natural swine -125-I-ACTH and of synthetic -131-I-ACTH were identical chromatographically and by saturation with iodine-125 and iodine-131, respectively, but differed by their behaviour in the organism. T1/2 for -125-I-ACTH (swine) was 4.7 min; the hormone was not incorporated into hepatic parenchyma, and only very weakly--into the kidneys, but it was intensively accumulated by the adrenal galnds. Radioactivity peak was recorded in the adrenal cortex 6 minutes after the administration of the labeled hormone. -131-I-ACTH (synthetic) disappeared from the blood with a falf-period of 11.2 min, was incorporated into the liver and particularly into the kidneys, and was not accumulated in the adrenal gland.
 ...
PMID:[A comparative analysis of the behavior of two labeled ACTH preparations in the body]. 16 77

The catalytic dehalogenation of iodinated derivatives of corticotropin in the presence of tritium was investigated. In 0.1 M acetic acid, complete and rapid removal of iodine was achieved in the presence of freshly prepared palladium or palladium oxide as catalyst, but the specific radioactivity of the product was only 10-20% of the theoretically attainable value. Synthetic human corticotropin containing a 3,5-diiodo tyrosine in position 23 in place of tyrosine was successfully dehalogenated in solvent mixture 0.1 M acetic acid: hexamethylphosphoramide: dimethylformamide (1 : 10 : 90, v/v) in the presence of palladium oxide and calcium carbonate. The product was obtained in 30% yield after purification by carboxymethyl cellulose chromatography. The tritiated hormone had a specific radioactivity of 46 Ci/mmol (80% of the theoretical value) and was as potent as synthetic human corticotropin in stimulating steroidogenesis and lipolysis.
 ...
PMID:Preparation and characterization of specifically tritiated adrenocorticotropin. 18 37

A 73-year-old woman was admitted to the hospital for severe persistent vomiting with fever, drowsiness, and weight loss. Elevated serum levels of thyroid hormones and the presence of a consciousness disorder with fever and vomiting led to the diagnosis of thyroid storm. A low normal concentration of serum cortisol, urinary 17-hydroxycorticosteroids and an elevated plasma level of corticotropin suggest that an inadequate adrenal reserve have been involved in the pathogenesis of the thyroid storm in this patient. She responded to the administration of intravenous methimazole and oral supersaturated potassium iodide solution.
 ...
PMID:Thyroid storm associated with probable subclinical hypoadrenocorticism in an elderly woman. 133 85

The human fetal adrenal gland exhibits a high rate of steroidogenesis during fetal development and produces the majority of steroids used by the placenta for estrogen synthesis. Corticotropin appears to be the principal hormonal regulator of steroidogenesis in the fetal adrenal gland. However, little is known concerning the regulation of corticotropin receptors. In this study we examined the long-term regulation of corticotropin responsiveness as measured by the ability of human fetal adrenal gland cells to produce cyclic adenosine monophosphate after corticotropin treatment for 3 hours. We also examined the regulation of corticotropin receptors as determined by iodine 125-labeled corticotropin binding to fetal adrenal cells. Fetal adrenal glands were obtained from second-trimester abortuses. The two distinct zones of the fetal adrenal gland, the definitive zone and the fetal zone, were separated and the tissue mechanically dispersed. Freshly isolated cells responded to corticotropin with a sevenfold to tenfold increase in the production of cyclic adenosine monophosphate, indicating a functional corticotropin receptor-adenylate cyclase coupling. However, when either fetal zone or definitive zone cells were grown and passed in monolayer culture, corticotropin stimulation of cyclic adenosine monophosphate production dropped to only twofold. The loss of corticotropin stimulation of cyclic adenosine monophosphate production occurred with a loss of the steroid-metabolizing enzyme 17 alpha-hydroxylase (P-450(17 alpha]. Because P-450(17 alpha) expression can be stimulated after treatment of fetal adrenal gland cells with corticotropin or forskolin, we attempted to increase the ability of corticotropin to stimulate cyclic adenosine monophosphate production in a similar manner. After cells were pretreated with corticotropin (0.1 to 100 nmol/L) or forskolin (0.1 to 100 mumol/L) for 4 days, their ability to produce cyclic adenosine monophosphate in response to corticotropin was examined. Pretreatment with both corticotropin and forskolin caused a dose-dependent increase in the ability of corticotropin to stimulate the production of cyclic adenosine monophosphate. Cells stimulated with corticotropin after pretreatment with forskolin exhibited a 35- to 50-fold increase in cyclic adenosine monophosphate production compared with nontreated cells (approximately twofold). Corticotropin pretreatment increased responsiveness to a lesser extent than forskolin pretreatment. The increase in corticotropin responsiveness occurred along with an induction of P-450(17 alpha) enzyme levels. The effect of pretreatment with corticotropin and forskolin on the binding of iodine 125-labeled corticotropin to definitive zone cells was also investigated. Corticotropin pretreatment increased corticotropin receptor binding 2.8 times; forskolin pretreatment increased corticotropin binding by seven times.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Regulation of corticotropin responsiveness in human fetal adrenal cells. 166 Oct 68

A variety of imaging procedures were performed in 28 patients with ectopic adrenocorticotropic hormone (ACTH) syndrome in an attempt to localize the ACTH-producing tumor. Diagnosis was made on the basis of removal of an ACTH-producing tumor or biopsy of metastases in the 19 patients with a proved source and the absence of ACTH gradients in bilateral samples of the inferior petrosal sinuses in the nine patients in whom an ACTH-secreting tumor had not been localized. Eleven bronchial carcinoids, two thymic carcinoids, three pheochromocytomas, and three islet-cell tumors constituted the proved sources. The condition has been cured in eight patients, six are alive with residual tumor, and five have died. Of the nine patients with undetected sites of ACTH production, one has died of pneumocystis pneumonia and eight are being treated medically or with bilateral adrenalectomy. Computed tomography (CT) of the chest and abdomen was the most helpful study in the detection of these tumors. Selective arteriography (bronchial and visceral), systemic and portal venous sampling, and iodine-131 meta-iodobenzylguanidine scintigraphy failed to demonstrate tumors when findings at CT were negative. Bronchial carcinoids constituted most of the ACTH-secreting tumors in this study (58%) and in a review of four large series (47%). To assure early detection of these potentially malignant tumors, pulmonary CT should be performed every 6 months, even after hypercortisolism has been medically or surgically controlled.
 ...
PMID:Ectopic adrenocorticotropic hormone syndrome: localization studies in 28 patients. 254 19

Corticotropin (ACTH) has two main actions in mammalian adrenal cortex: acute stimulation of glucocorticoids secretion and trophic effect which allow the expression of genes encoding for the steroidogenic enzymes. The ACTH membrane bound receptor was one of the first to be demonstrated by direct binding of labeled hormone to subcellular preparations of the adrenal cortex. However, detection and characterization of physiological relevance to ACTH receptors has been difficult, because of the low biological activity of the labeled ACTH. Introduction of a bulky iodine atom into Tyr2 and the oxidation of Met4 appear to contribute most to the loss of activity. These difficulties were overcome recently by using an [125I]-ACTH labeled only in Tyr23, which retains full biological activity. Using this labeled hormone, physiologically relevant ACTH receptors, with high affinity (KD congruent to 10-10M) and low capacity (congruent to 2000 sites/cell) have been characterized in several mammals. A second site of low affinity (KD congruent to 10(-7M) and high capacity, has been found in some studies but the significance of this second site is unknown since it cannot be related to any physiological response of adrenal cells to ACTH. In contrast with the loss of receptors and desensitization of target cells caused by most polypeptide hormones, ACTH seems to regulate positively its own receptors and the cAMP response. The molecular weight of the ACTH receptor appears to be between 83 and 100 KD.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[ACTH receptors]. 255 6

The blood-brain barrier is capable of transporting peptides with anti-opiate (Tyr-MIF-1) and opiate (enkephalins) activity out of the central nervous system. The relationship of this transport system to the various actions of opiates remains unexplored. This study examined the relationship between the rate of transport and opiate-induced analgesia. Both restraint, a stress that provokes an opiate-mediated analgesia, and the administration of morphine (12 mg/kg, i.p.) each induced an inhibition in the rate of transport. Such inhibition exhibited specificity, since the saturable, brain to blood transport of iodide remained unaltered. However, it was possible to dissociate analgesia and inhibition of transport. The onset and peak of analgesia, as measured by tail-flick latency induced by morphine, preceded the onset and peak of the inhibition of transport. Naltrexone, which blocks opiate-mediated analgesia, also induced inhibition of transport without any significant effect on tail-flick latency. (-) Naloxone but not (+) naloxone also weakly inhibited transport. Deprivation of food and water, associated with analgesia possibly mediated by the opiate, beta-endorphin, which is not transported out of the brain by this system, did not alter transport. These results suggest that while inhibition of transport and analgesia may occur together, these events probably represent two separate aspects of the action of opiates, that may even be mediated by separate receptor sites or peptides in the opiate family.
 ...
PMID:Analgesia and the blood-brain barrier transport system for Tyr-MIF-1/enkephalins: evidence for a dissociation. 289 31

Hormones are extracted from plasma with varying efficiency. Thus, markers or internal standards are often needed, to monitor and correct for extraction losses. To do so is difficult in the case of peptide hormones because radioactive recovery markers either have a low specific activity or, if labeled with iodine, may not be fully representative because of alterations in their size and charge. More importantly, markers labeled with 125I can interact in, and thus compromise, the subsequent radioimmunoassay. AtT-20 mouse pituitary tumor cells, which can be stimulated to synthesize and secrete pro-opiomelanocortin peptides, can biosynthetically label beta-lipotropin (beta-LPH) with [35S]methionine. The labeled peptide, which is co-eluted with unlabeled beta-LPH in "high-performance" liquid chromatography, is fully immunoprecipitable and has a specific activity of 34 Ci/g. We use this labeled peptide to monitor the recovery of beta-LPH in silicic acid extraction from plasma. This peptide is an ideal marker of analytical recovery because it does not interfere in subsequent radioimmunoassays.
 ...
PMID:Biosynthesized [35S]methionine-labeled pro-opiomelanocortin peptides as novel recovery markers in radioimmunoassay of peptide hormones. 293 87

The central nervous system may be highly susceptible to the toxic effects of contrast media (CM). Previous experiments demonstrated that vasopressin is released after the intravenous administration of CM. The present study examined the response of the opiocortin system to CM. Neurons of the rat basal hypothalamus, dispersed and attached to Cytodex-3 beads, were perfused with sodium diatrizoate, metrizamide or iohexol (3 mg iodine/ml). The effluent was collected, and the beta-endorphin (B-E) content was measured by a radioimmunoassay technique. Results, normalized to the internal positive control, were compared with release from normal saline (negative control) by analysis of variance. Diatrizoate and metrizamide caused significant release of B-E (p less than 0.03). Iohexol did not stimulate release of B-E. These results suggest that diatrizoate and metrizamide, but not iohexol, can stimulate the release of hormones from hypothalamic neurons. The phenomenon may play a role in some reactions to intravascular CM administration since these neurons are not protected by a blood-brain barrier.
 ...
PMID:Effect of contrast media on beta-endorphin secretion. An in vitro study. 297 39

Our attempts to develop adrenocorticotropic hormone (ACTH) analogues that can be employed for ACTH receptor identification and isolation began with the synthesis of ACTH fragments containing N epsilon-(dethiobiotinyl)lysine (dethiobiocytin) amide in position 25 to be used for affinity chromatographic purification of hormone-receptor complexes on Sepharose-immobilized avidin resins. Because labeling ACTH or ACTH fragments by conventional iodination techniques destroys biological activity due to oxidation of Met4 and incorporation of iodine into Tyr2, we have prepared [Phe2,Nle4]ACTH1-24, [Phe2,Nle4,biocytin25]ACTH1-25 amide, and [Phe2,Nle4,dethiobiocytin25]ACTH1-25 amide by conventional synthetic techniques. The HPLC profiles and amino acid analyses of the final products indicate that the materials are of a high degree of purity. The amount of tertiary butylation of the Trp residue in the peptides was assessed by NMR and was found to be less than 0.5%. All three peptides are equipotent with the standard ACTH1-24 as concerns their ability to stimulate steroidogenesis and cAMP formation in bovine adrenal cortical cells. Iodination of [Phe2,Nle4]ACTH1-24, with iodogen as the oxidizing agent, has been accomplished without any detectable loss of biological activity. The mono- and diiodo derivatives of [Phe2,Nle4]ACTH1-24 have been prepared, separated by HPLC, and assayed for biological activity. Both peptides have the full capacity to stimulate steroidogenesis and cAMP production in bovine adrenal cortical cells.
 ...
PMID:Radioactive probes for adrenocorticotropic hormone receptors. 300 27


1 2 3 4 5 Next >>