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)

The oxidative burst of rainbow trout (Oncorhynchus mykiss) phagocytes was previously found to be differentially modulated by adrenocorticotropic hormone (ACTH) and the catecholamine receptor agonists phenylephrine and isoproterenol. From data obtained using both luminol-enhanced chemiluminescence (LECL) and ferricytochrome C (cyt C) reduction to measure oxidative burst kinetics, we postulated that the observed modulation was mediated by affects on enzymes responsible for the production and metabolism of superoxide anion. Using exogenous superoxide dismutase (SOD) and catalase as scavengers, nitroprusside to poison endogenous SOD, and an assay for hydrogen peroxide, we have tested our postulates by exploiting the differences with which various reactive oxygen intermediates influence LECL and cyt C reduction. The ability of ACTH to potentiate both assays of the oxidative burst appears due to its enhancing influence on the production of superoxide. Phenylephrine, an alpha-adrenergic receptor agonist, appears to enhance the activity of endogenous SOD, whereas isoproterenol, a beta-adrenergic receptor agonist, may suppress SOD activity. This work reveals how components of the natural immune system may be regulated by products of the neuroendocrine system. Also, lymphocyte-derived ACTH may provide a novel pathway for lymphoid regulation of inflammation.
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PMID:Modulation of the oxidative burst in trout myeloid cells by adrenocorticotropic hormone and catecholamines: mechanisms of action. 165 72

Culturing sympathetic ganglion neurons in vitro may modify phenotypic expression of some neurotransmitters. For dorsal root ganglia (DRG), contradictory results have been reported; most studies have used immature material. We have therefore performed a detailed immunocytochemical analysis of the transmitter content of cultured adult rat DRG neurons. To demonstrate possible modifications of neurotransmitter phenotypes, we have compared the results obtained with the same techniques on neurons cultured for 3 days and on freshly dissociated DRG cells. Also, the transmitter profile of cultured neurons was compared with that known from in situ studies. Out of 22 antigens studied, 20 were detected in cultured DRG neurons. All of them were expressed in small and/or intermediate-sized cells. Large neurons only contained CGRP, VIP, NPY, beta-END, ENK, and GABA. The percentage of immunostained neurons varied for the various antisera: less than 10% of cultured neurons were positive for ENK, beta-LPH, beta-END, DYN, VASO, and OXY; 10-30% for SOM, CCK, CAT, and SP; and greater than 30% for NPY, CRF, GLU, NT, VIP, GABA, GRP, CGRP, 5-HT, and TRH. In the latter two groups of transmitters (except CGRP), the proportion of immunoreactive neurons was by far larger in cultured than in freshly dissociated DRG. The most pronounced (greater than 25%) increase in the proportion of positively stained neurons after culturing was observed for the GRP, CRF, TRH, and 5-HT antisera. Serotonin was the only transmitter identified in cultured but not in freshly dissociated cells. These data indicate, on one hand, that various antigens, for example, CAT, GABA, NT, TRH, NPY, beta-LPH, and beta-END, which up to now have not been described in DRG in situ, can be detected immunocytochemically a few hours after dissociation of adult rat DRG. On the other hand, several transmitters, for example, VIP, NPY, SP, GABA, GLU, NT, GRP, CRF, TRH, and 5-HT, are expressed in a significantly higher proportion of cells in cultured than in freshly dissociated preparations. This might reflect a change in the phenotypic expression of transmitters due to the new environment generated by the culture conditions, a hypothesis that can be tested by measuring specific mRNA levels. Moreover, considering the plasticity and multipotentiality of their transmitter phenotype, cultured adult DRG neurons might represent an interesting material for autografts into the injured central nervous system.
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PMID:Neurotransmitter phenotype plasticity in cultured dissociated adult rat dorsal root ganglia: an immunocytochemical study. 256 40

Opioid peptides have been shown to modulate the function of cells associated with host defense. Both opiate and nonopiate receptor mechanisms have been shown to mediate cell responses to these peptides. In this study we used a ferricytochrome C reduction microassay to measure superoxide (O2-) production by human polymorphonuclear leukocytes after stimulation with beta-endorphin (beta-END). beta-END was found to stimulate O2- release at concentrations from 10(-14) to 10(-8) M; the peak response occurred at 10(-12) M. A microassay based on the horseradish peroxidase-mediated oxidation of phenol red was used to demonstrate the production of hydrogen peroxide H2O2, by beta-END at 10(-12) M. The accumulation of H2O2 was reduced by the inhibitor, nitroprusside, and by the converting enzyme, catalase. The accumulation of O2- in response to the potent chemotactic peptide formyl-methionine-leucine-phenylalanine was studied and a distinctly different dose-response profile with a peak response at 10(-8) M was observed. Because beta-END can apparently bind to and activate cellular functions by nonopiate receptors, N-acetyl-beta-END was tested. At doses between 10(-14) and 10(-8) M, it failed to effect O2- accumulation. Moreover, (-)-naloxone 10(-12) M was shown to completely abolish the stimulatory effect of equimolar beta-END whereas (+)-naloxone was entirely ineffective. At 10(-8) M both stereoisomers also failed to inhibit formyl-methionine-leucine-phenylalanine 10(-8) M. Thus, at the picomolar concentration present in the human systemic circulation, beta-END activates oxygen metabolism by polymorphonuclear leukocytes through stereoselective, naloxone-sensitive opiate receptors.
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PMID:Beta-endorphin stimulates human polymorphonuclear leukocyte superoxide production via a stereoselective opiate receptor. 303 21

The effects of dithiothreitol on basal glucose oxidation, hormone-induced lipolysis and insulin receptors in isolated rat adipocytes were studied. Dithiothreitol produced a dose-dependent stimulation of basal glucose oxidation and inhibition of adrenaline-induced lipolysis. Dithiothreitol also inhibited corticotropin-induced lipolysis, but failed to inhibit dibutyryl cyclic AMP-induced lipolysis. Dithiothreitol did not inhibit the binding of the beta-adrenergic antagonist [3H]dihydroalprenolol to adipocytes. Neither catalase (100 micrograms/ml) nor EDTA (2 mM) abolished the antilipolytic effect of dithiothreitol. Treatment of isolated adipocytes with 1 mM-dithiothreitol for 20 min at 37 degrees C also caused stimulation of basal glucose oxidation and inhibition of adrenaline-induced lipolysis. A Scatchard plot of insulin binding to control adipocytes was curvilinear. However, treatment of cells with 1 mM-dithiothreitol decreased the curvilinearity of the plot, indicating that only a low-affinity state of the insulin receptors exists in the dithiothreitol-treated adipocytes. These findings suggest that the insulin-like activities of dithiothreitol are mediated through the interaction of dithiothreitol with insulin receptors.
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PMID:Insulin-like effects of dithiothreitol on isolated rat adipocytes. 704 94

Previously, we have shown that low doses of ethanol (12.5-100 mM) and acetaldehyde (12.5-50 microM), but not salsolinol, enhanced immunoreactive beta-endorphin (IR-beta-EP) secretion from fetal hypothalamic neurons in primary culture. In this study, the effects of ethanol, propanol, and butanol, as well as the effect of catalase inhibitors on IR-beta-EP secretion were studied in vitro to determine the role of membrane fluidization and ethanol metabolism on ethanol-induced IR-beta-EP secretion. The primary cultures of fetal hypothalamic neurons were maintained for 8-9 days in chemically defined medium and treated for 5 hr with ethanol (50 mM), propanol (25 and 50 mM), and butanol (25 and 50 mM). Determination of hourly secretion of IR-beta-EP from the cultures revealed that only 50 mM ethanol caused stimulation of IR-beta-EP secretion, whereas propanol and butanol did not alter IR-beta-EP response at any given concentration. Pretreatment of these cultures with the catalase inhibitors, 3-amino-1,2,4-triazole (3-AT; 1, 5, and 10 mM), caused a dose-dependent inhibition of ethanol-stimulated IR-beta-EP secretion, but did not inhibit dibutyryl cAMP (dcAMP)-stimulated IR-beta-EP secretion. Another catalase inhibitor, sodium azide (5 mM), also inhibited ethanol-stimulated IR-beta-EP secretion. Measurement of acetaldehyde production in cultured cells and media after ethanol or dcAMP treatments revealed that cultured cells produce acetaldehyde only after ethanol treatment and at levels of acetaldehyde (8-24 microM) that are known to evoke IR-beta-EP release. The catalase inhibitor 3-AT (10 mM) treatment reduced ethanol-evoked acetaldehyde production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of ethanol, propanol, butanol, and catalase enzyme blockers on beta-endorphin secretion from primary cultures of hypothalamic neurons: evidence for a mediatory role of acetaldehyde in ethanol stimulation of beta-endorphin release. 762 66

Treatment of human HaCaT keratinocytes with corticotropin-releasing hormone modulates cell proliferation and expression of inflammation markers. In this study we report that corticotropin-releasing hormone also inhibits nuclear factor-kappaB binding and transcriptional activity. Incubating cells in the absence of growth factors increased nuclear factor-kappaB activity; this effect was significantly attenuated by corticotropin-releasing hormone. Specifically, corticotropin-releasing hormone downregulated p50/p50 and p50/p65 dimers of nuclear factor-kappaB, diminished kappaB-driven CAT reporter gene activity and inhibited IkappaB-beta degradation. Moreover, corticotropin-releasing hormone inhibited the trans-cription of the nuclear factor-kappaB responsive genes, interleukin-2 and heat shock protein 90.
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PMID:Corticotropin-releasing hormone inhibits nuclear factor-kappaB pathway in human HaCaT keratinocytes. 1467 1

The radioactive and thermal effects of radon hot spring were biochemically compared under a sauna room or hot spring conditions with a similar chemical component, using the parameters that are closely involved in the clinic for radon therapy. The results showed that the radon and thermal therapy enhanced the antioxidation functions, such as the activities of superoxide dismutase (SOD) and catalase, which inhibit lipid peroxidation and total cholesterol produced in the body. Moreover the therapy enhanced concanavalin A (ConA)-induced mitogen response and increased the percentage of CD4 positive cells, which is the marker of helper T cells, and decreased the percentage of CD8 positive cells, which is the common marker of killer T cells and suppressor T cells, in the white blood cell differentiation antigen (CD8/CD4) assay. Furthermore, the therapy increased the levels of alpha atrial natriuretic polypeptide (alpha ANP), beta endorphin, adrenocorticotropic hormone (ACTH), insulin and glucose-6-phosphate dehydrogenase (G-6-PDH), and it decreased the vasopression level. The results were on the whole larger in the radon group than in the thermal group. The findings suggest that radon therapy contributes more to the prevention of life-style-related diseases related to peroxidation reactions and immune suppression than to thermal therapy. Moreover, these indicate what may be a part of the mechanism for the alleviation of hypertension, osteoarthritis (pain), and diabetes mellitus brought about more by radon therapy than by thermal therapy.
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PMID:Biochemical comparison between radon effects and thermal effects on humans in radon hot spring therapy. 1513 94

It is suggested that some of the behavioral effects of ethanol, including its psychomotor properties, are mediated by beta-endorphin and opioid receptors. Ethanol-induced increases in the release of hypothalamic beta-endorphin depend on the catalasemic conversion of ethanol to acetaldehyde. Here, we evaluated the locomotor activity in rats microinjected with ethanol directly into the hypothalamic arcuate nucleus (ArcN), the main site of beta-endorphin synthesis in the brain and a region with high levels of catalase expression. Intra-ArcN ethanol-induced changes in motor activity were also investigated in rats pretreated with the opioid receptor antagonist, naltrexone (0-2 mg/kg) or the catalase inhibitor 3-amino-1,2,4-triazole (AT; 0-1 g/kg). We found that ethanol microinjections of 64 or 128, but not 256 microg, produced locomotor stimulation. Intra-ArcN ethanol (128 microg)-induced activation was prevented by naltrexone and AT, whereas these compounds did not affect spontaneous activity. The present results support earlier evidence indicating that the ArcN and the beta-endorphinic neurons of this nucleus are necessary for ethanol to induce stimulation. In addition, our data suggest that brain structures that, as the ArcN, are rich in catalase may support the formation of ethanol-derived pharmacologically relevant concentrations of acetaldehyde and, thus be of particular importance for the behavioral effects of ethanol.
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PMID:Ethanol injected into the hypothalamic arcuate nucleus induces behavioral stimulation in rats: an effect prevented by catalase inhibition and naltrexone. 1879 46

Exposure of cultured human melanocytes to ultraviolet radiation (UV) results in DNA damage. In melanoma, UV-signature mutations resulting from unrepaired photoproducts are rare, suggesting the possible involvement of oxidative DNA damage in melanocyte malignant transformation. Here we present data demonstrating immediate dose-dependent generation of hydrogen peroxide in UV-irradiated melanocytes, which correlated directly with a decrease in catalase activity. Pretreatment of melanocytes with alpha-melanocortin (alpha-MSH) reduced the UV-induced generation of 7,8-dihydro-8-oxyguanine (8-oxodG), a major form of oxidative DNA damage. Pretreatment with alpha-MSH also increased the protein levels of catalase and ferritin. The effect of alpha-MSH on 8-oxodG induction was mediated by activation of the melanocortin 1 receptor (MC1R), as it was absent in melanocytes expressing loss-of-function MC1R, and blocked by concomitant treatment with an analog of agouti signaling protein (ASIP), ASIP-YY. This study provides unequivocal evidence for induction of oxidative DNA damage by UV in human melanocytes and reduction of this damage by alpha-MSH. Our data unravel some mechanisms by which alpha-MSH protects melanocytes from oxidative DNA damage, which partially explain the strong association of loss-of-function MC1R with melanoma.
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PMID:alpha-MSH activates immediate defense responses to UV-induced oxidative stress in human melanocytes. 1965 42

Local or 'Immune' Corticotropin-Releasing Hormone (CRH) is secreted in peripheral tissues and plays a direct immunomodulatory role as an endocrine or paracrine mediator of inflammation. The present study was undertaken to determine whether CRH affects the endothelial redox state. Accordingly, intracellular reactive oxygen species (ROS) content and peroxynitrite levels, endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) levels as well as catalase activity, superoxide dismutase (SOD) activity and glutathione (GSH) levels were measured in the presence or absence of selective CRH receptor-1 and CRH receptor-2 inhibitors in endothelial EAhy926 cells exposed in vitro in 10(-7) M CRH for 2 h. CRH acting through both receptors induced a significant increase of ROS content (p < 0.001), catalase activity (p < 0.001) and SOD activity (p < 0.001), accompanied by a simultaneous significant decrease of eNOS activity and NO levels (p < 0.001), as well as a significant increase in nitrotyrosine (peroxynitrite) levels (p < 0.05). The data indicate that CRH may act as a regulator of pro-inflammatory mechanisms inducing adaptation of endothelial cell function to local stress.
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PMID:Effect of CRH on NO bioavailability, ROS production and antioxidant defense systems in endothelial EAhy926 cells. 2052 75


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