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

Beta-endorphin (beta-ED) levels were evaluated in blood and seminal plasma of men with infertility due to varicocele, obstructive and nonobstructive azoospermia, and idiopathic oligoasthenospermia. The relation of this opiate to serum levels of gonadotropins, prolactin, testosterone, androstenedione, and dehydroepiandrosterone sulfate has also been investigated. beta-ED levels in seminal plasma were significantly higher than in blood plasma (p less than 0.001) in all persons studied. No statistically significant differences were found for beta-ED concentrations in semen or blood among any of the infertility situations studied. Nor were significant correlations observed between the concentration of this opiate and that of gonadotropins, prolactin, and androgens. The measurement of beta-ED in semen has little value in the differential diagnosis of male infertility. Nonetheless, its presence in high levels in semen must have some unknown function. Possibly, it comes from the various sites of the male reproductive tract, since no significant differences were found between obstructive and nonobstructive azoospermias.
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PMID:Beta-endorphin and male infertility. 294 70

Neurotensin (NT) differentially altered ethanol-induced anesthesia as measured by duration of loss of righting response or by blood ethanol levels producing loss of righting response in mice (LS and SS) which were selectively bred for differences in response to ethanol. At doses of 5-500 ng i.c.v., NT increased ethanol sensitivity in SS mice, but not in LS mice, as measured by blood ethanol concentrations at loss of righting response. At higher doses, 0.5-10 micrograms i.c.v., NT enhanced the sensitivity of both SS and LS mice to ethanol-induced anesthesia. The hypothermic effect of ethanol determined at loss of righting response was not altered in either LS or SS mice at low doses of NT, but at higher doses NT enhanced ethanol-induced hypothermia in both lines of mice. The altered anesthetic sensitivity was specific for ethanol in that NT did not alter pentobarbital-induced sleep time in either LS or SS mice and halothane anesthesia was altered slightly only in LS mice. NT analogues, N-acetyl-NT8-13, and [D-Trp11]-NT but not NT1-8 enhanced the anesthetic action of ethanol in SS mice. Bombesin, cholecystokinin sulfate, substance P, [D-Trp8, D-Cys14]-somatostatin and corticotropin releasing hormone (CRF) were not effective in enhancing ethanol-induced anesthesia in LS or SS mice. CRF appeared to decrease ethanol sensitivity in LS but not in SS mice. Beta-Endorphin (beta-END) markedly increased the ethanol sensitivity of SS and to a lesser extent of LS mice at relatively high doses, e.g. 0.5-1.0 micrograms i.c.v. The results of the present study indicate that differences in brain sensitivity of LS and SS mice to ethanol may be mediated by genetic differences in NT systems. Likewise, NT, and probably beta-endorphin, may interact with other neurochemical processes that are involved in the mechanism of ethanol-induced anesthesia and that differ genetically in LS and SS mice.
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PMID:Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. 294 96

Cationized albumin (pI greater than 8), unlike native albumin (pI approximately 4), enters cerebrospinal fluid (CSF) rapidly from blood. This suggests that a specific uptake mechanism for cationized albumin may exist at the brain capillary wall, i.e. the blood-brain barrier. Isolated bovine brain capillaries rapidly bound cationized [3H]albumin and approximately 70% of the bound radioactivity was resistant to mild acid wash, which is assumed to represent internalized peptide. Binding was saturable and a Scatchard plot gave a maximal binding capacity (Ro) = 5.5 +/- 0.7 micrograms/mgp (79 +/- 10 pmol/mgp), and a half-saturation constant (KD) = 55 +/- 8 micrograms/ml (0.8 +/- 0.1 microM). The binding of cationized [3H]albumin (pI = 8.5-9) was inhibited by protamine, protamine sulfate, and polylysine (molecular weight = 70,000) with a Ki of approximately 3 micrograms/ml for all three proteins. The use of cationized albumin in directed delivery of peptides through the blood-brain barrier was examined by coupling [3H]beta-endorphin to unlabeled cationized albumin (pI = 8.5-9) using the bifunctional reagent, N-succinimidyl 3-(2-pyridyldithio)proprionate. The [3H]beta-endorphin-cationized albumin chimeric peptide was rapidly bound and endocytosed by isolated bovine brain capillaries, and this was inhibited by unlabeled cationized albumin but not by unconjugated beta-endorphin or native bovine albumin. Cationized albumin provides a new tool for studying absorptive-mediated endocytosis at the brain capillary and may also provide a vehicle for directed drug delivery through the blood-brain barrier.
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PMID:Absorptive-mediated endocytosis of cationized albumin and a beta-endorphin-cationized albumin chimeric peptide by isolated brain capillaries. Model system of blood-brain barrier transport. 295 63

The role of skeletal muscle thermogenesis (increases in skeletal muscle tone) in the hyperthermic responses of conscious, unrestrained rats given acute or repeated i.p. or i.c.v. injections of morphine sulfate (MS) or beta-endorphin was investigated. Initial blood gas experiments showed that rats given acute i.p. injections of MS caused PO2 and pH to decrease by 60 min postadministration in a dose-related fashion whereas PCO2 increased; with repeated MS administration the respiratory acidosis seen with acute injections was reduced. Acute i.p. injections of MS (1, 10 or 20 mg/kg) caused catalepsy scores, plasma lactate levels and electromyographic (EMG) amplitude to be elevated in a dose-related fashion along with a rise in rectal temperatures (TRS). Surface (tail) temperatures also rose after the acute MS injections but only after the increase in TR. Significant increases in EMG amplitude after acute injections of MS occurred even before TRS increased and, with subsequent naloxone HCl administration (10 mg/kg i.p.), a rapid and marked fall in EMG amplitude occurred before TRS fell back to saline control levels. Acute i.c.v. injections of 1.1 nmol of either MS or beta-endorphin also caused EMG amplitudes to rise significantly before TRS began to increase. Tail temperatures again increased passively after i.c.v. injection of either drug. Subsequent naloxone injections (10 mg/kg i.p.) to these groups also caused EMG amplitudes to decrease before TRS decreased back to control TRS. Repeated i.p. injections of MS (10 mg/kg i.p. daily for 5 days) caused TRS to be higher than those seen after the initial injection but catalepsy scores, plasma lactates and EMG amplitudes were below those respective levels seen upon acute MS administration. Similar chronic findings occurred in other groups of rats given 1.1 nmol of either MS or beta-endorphin i.c.v., when they had been previously given repeated i.p. injections of MS (5 mg/kg i.p. twice daily for 2 days). The results indicate that acute peripheral or central injections of MS or beta-endorphin to conscious rats cause skeletal muscle to be activated, resulting in nonlocomotor, catatonic behavior. This skeletal muscle activation occurs before the rise in TR and is thought to be an important and possibly the primary cause of the resultant hyperthermia seen in rats after acute central or peripheral administration of MS or beta-endorphin. Repeated injections of morphine cause TRS to escalate higher, compared to that seen with acute MS administration, yet catalepsy scores, plasma lactate levels and EMG amplitude changes did not increase likewise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Skeletal muscle thermogenesis: its role in the hyperthermia of conscious rats given morphine or beta-endorphin. 295 69

In the present study, baboon fetal adrenal cells were obtained at mid- and late gestation and incubated for various intervals to determine simultaneously the effects of length of incubation and stage of development on the pattern of adrenal steroidogenesis. Cells were treated with adrenocorticotropic hormone (ACTH) from 0 to 48 h of incubation, and the concentrations of dehydroepiandrosterone (DHA), DHA-sulfate (DHAS), and androstenedione (delta 4A) were determined in the medium. The secretion of DHA and DHAS by untreated or ACTH-treated cells of midgestation increased linearly throughout the 48-h incubation period. In fetal adrenal incubates of late gestation, however, DHA and DHAS concentrations peaked at 3 h and declined thereafter, suggesting that the DHA secreted into the medium was further metabolized by this tissue. Baboon fetal adrenal cells formed similar amounts of DHAS and DHA at midgestation, but greater quantities of DHAS were formed at term. In fetal adrenal incubates of midgestation, DHA concentrations exceeded those of delta 4A by threefold, a relationship which was reversed at late gestation, probably due to the increase in the activity of 3 beta-hydroxy-steroid dehydrogenase with advancing gestation. Because the decline in DHA with time of incubation was also associated with a concomitant decrease in DHAS and no change in delta 4A, it does not appear that formation of these steroids account for the loss of DHA. We conclude that the pattern of androgen metabolism exhibited by fetal adrenal cells obtained at midgestation is different from that at term.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in the pattern of androgen formation in vitro by the baboon fetal adrenal gland at mid- and late gestation. 296 75

To determine the locus of opiate modulation of ACTH secretion, 11 normal subjects were given ovine corticotropin-releasing hormone (CRH) 30 min after receiving either placebo or morphine sulfate. Plasma ACTH, cortisol, arginine vasopressin (AVP), epinephrine, norepinephrine, and CRH were measured 30 min before and up to 150 min after CRH administration. Morphine blunted the ACTH response for the first 60 min and cortisol response for the first 90 min after CRH administration. Morphine did not lower arginine vasopressin or catecholamine levels. To determine whether morphine's effect on ACTH and cortisol was due to a direct action on the corticotroph cell, dispersed rat pituitary cells were perifused with medium containing 1 microgram/ml morphine sulfate or medium alone. Morphine had no effect on the ACTH response of these cells to 10 nM CRH pulses. Similarly, morphine had no effect on ACTH production by dispersed rat pituitary cells in monolayer culture in response to 90- and 180-min incubations with 5 nM CRH. We conclude that morphine blunts the early response of the pituitary gland to CRH in vivo. Based on the lack of a direct effect of morphine on rat pituitary cells in vitro, we postulate that morphine given in vivo may modulate the pituitary ACTH response to CRH through other suprapituitary factors.
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PMID:Morphine inhibits the pituitary-adrenal response to ovine corticotropin-releasing hormone in normal subjects. 298 35

A photoaffinity reagent 2-nitro-4-azidophenylsulfenyl chloride (2,4-NAPS-Cl) and synthetic analogs of human beta-endorphin (beta h-EP) were employed to demonstrate the presence of receptor sites specific for beta h-EP but of non-opioid character in a human neuroblastoma cell line (IMR-32). The radioactive photoaffinity probe was carried out using [125I-Tyr1,2,4-NAPS-Trp27]-beta h-EP and IMR-32 cell membranes. After solubilization with sodium dodecyl sulfate (SDS) and SDS polyacrylamide gel electrophoresis, a single labelled protein band was identified with a molecular weight of 72,000. Labelling was blocked by beta h-EP or beta h-EP-(6-31) but remained in the presence of beta h-EP-(1-27). The specificity of this band is thus identical to that of the non-opioid site previously characterized. Various nonionic or zwitterionic detergents did not extract the labelled non-opioid site.
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PMID:Beta-endorphin: photoaffinity labelling of a non-opioid binding site in a human neuroblastoma. 298 33

125I-beta-Endorphin (human) binds with high affinity, specificity, and saturability to rat brain and neuroblastoma X glioma hybrid cell (NG 108-15) membranes. Dissociation constants and binding capacities were obtained from Scatchard plots and are 2 nM and 0.62 pmol/mg of protein for rat whole brain and 6 nM and 0.8 pmol/mg of protein for NG 108-15 cells. Results from competition experiments also indicate that this ligand interacts with high affinity with both mu and delta opioid binding sites, with a slight preference for mu sites, while exhibiting low affinity at kappa sites. We have demonstrated that human 125I-beta-endorphin is a useful probe for the investigation of the subunit structure of opioid receptors. The specific cross-linking of this ligand has revealed the presence of four reproducible bands or areas after sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography at 65, 53, 38, and 25 kDa. All labeled bands seem to be opioid receptor related since they are eliminated when binding is carried out in an excess of various opiates. The evidence we have obtained using rat whole brain (delta congruent to mu), rat thalamus (largely mu), bovine frontal cortex (delta:mu congruent to 2:1), and NG 108-15 cells (delta) demonstrates that different labeling patterns are obtained when mu and delta binding sites are cross-linked. The pattern obtained on sodium dodecyl sulfate-polyacrylamide gel electrophoresis from cross-linked mu sites contains a major (heavily labeled) component of 65 kDa and a minor component of 38 kDa, while patterns from delta sites contain a major labeled component of 53 kDa. This 53-kDa band appears clearly in extracts from NG 108-15 cells and bovine frontal cortex, while in rat whole brain a diffusely labeled region is present between 55 and 41 kDa. In addition, NG 108-15 cells also display a minor labeled component at 25 kDa. The relationship of the minor bands to the major bands is not clear.
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PMID:Covalent labeling of opioid receptors with radioiodinated human beta-endorphin. Identification of binding site subunit. 299 92

To determine the direct effect of prolactin on adrenal androgen secretion, the daily secretions of dehydroepiandrosterone sulfate (DHEA-S), dehydroepiandrosterone (DHEA), androstenedione and cortisol were determined in monolayer culture of bovine adrenal cells in the presence or absence of adrenocorticotropic hormone (ACTH) and/or prolactin. In the absence of ACTH ovine prolactin alone had no effect on steroid secretion during seven-day culture. Ovine prolactin, when administered in combination with ACTH, significantly potentiated the stimulatory effect of ACTH on DHEA-S and DHEA but not androstenedione secretion on the seventh day in culture. On the first day in culture prolactin showed no synergistic effect with ACTH on DHEA and DHEA-S secretion, although ACTH significantly increased DHEA and cortisol secretion. DHEA-S secretion increased as a function of prolactin concentration in the presence of ACTH. These results indicated that long-term treatment by ovine prolactin with ACTH caused the increase in adrenal androgen secretion from bovine adrenal cells. The site of action of prolactin was suggested to be the partial inhibition of adrenal 3 beta-hydroxysteroid dehydrogenase by the result of increases in DHEA-S and DHEA but not androstenedione secretion.
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PMID:Ovine prolactin potentiates the action of adrenocorticotropic hormone on the secretion of dehydroepiandrosterone sulfate and dehydroepiandrosterone from cultured bovine adrenal cells. 299 21

Factors other than adrenocorticotropic hormone (ACTH) are thought to influence fetal adrenal steroidogenesis during primate pregnancy. Therefore, we determined the effects of prolactin (Prl), growth hormone (GH), and human chorionic gonadotropin (hCG) as well as ACTH on steroid secretion by collagenase-dispersed baboon fetal adrenal cells. Adrenal glands were obtained from seven baboon (Papio anubis) fetuses following cesarean section at Day 100-107 of gestation (term = Day 184). Tissue was minced with a fine scissors and cells were dispersed with 0.2% collagenase, then washed with Medium 199 containing penicillin/streptomycin. Cells (0.5 X 10(4)) were placed in 4 ml Medium 199 with or without 10 nmol ovine Prl, ovine GH, or ACTH, or 50 nmol hCG. After 18 h incubation (37 degrees C), cells were separated by centrifugation and the quantities of cortisol (F), dehydroepiandrosterone (DHA), and DHA-sulfate (DHAS) secreted into the medium were determined. In controls, DHA secretion [224 +/- 96 ng/(24 h X 10(5) cells] was greater (P less than 0.05) than that of DHAS (20 +/- 12) and F (14 +/- 12). Adrenocorticotropic hormone, Prl, and GH stimulated (P less than 0.05) DHA secretion by 370% +/- 71%, 215% +/- 61%, and 292% +/- 73%, respectively; hCG was not effective. Due primarily to the relatively low secretion rates, DHAS and F secretion were not altered by hormonal treatment. Moreover, addition of 20 nmol progesterone to the medium in the presence or absence of ACTH did not influence F production. These findings indicate that the baboon fetal adrenal at midgestation does not utilize placental progesterone for F synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of baboon fetal adrenal androgen production by adrenocorticotropic hormone, prolactin, and growth hormone. 299 43


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