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 relationship between the neuropeptides leu-enkephalin, met-enkephalin, kentsin (a contraceptive tetrapeptide) and ethanol was studied in the male rat. This was pursued by assessing the effect of these peptides and some of their amino acid constituents on voluntary drinking of ethanol by rats with preference to alcohol intake. The in vitro effect of some of kentsin amino acids constituents on rat liver alcohol and aldehyde dehydrogenase was also studied. Intraperitoneal injection of leu-enkephalin, but not met-enkephalin, produced a delayed increase in voluntary ethanol drinking by the rat. Injection of identical doses of kentsin produced a much lesser effect than the leu-enkephalin treatment. The separate or combined treatment with phenylalanine and leucine, resulted in decreased voluntary consumption of ethanol. Coadministration of glycine or tyrosine alone or both combined did not influence ethanol drinking. Coadministration of tyrosine or glycine with leucine negated the leucine effect on ethanol drinking. Both L-arginine and L-proline, the two amino acids component of kentsin, decreased the specific activity of rat liver mitochondrial aldehyde dehydrogenase in vitro at 10(-3) mol concentration. The results suggest an interrelationship between the peptides studied and ethanol preference. The data also indicates that some of kentsin action on ethanol drinking may be related to the effect of some of its degradation product on hepatic ethanol-derived acetaldehyde metabolism and/or may be related to the endocrine property of kentsin.
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PMID:Enkephalins, their constituents and voluntary drinking of ethanol by the rat. 281 54

To understand the mechanism by which peptide antigens are processed and presented to T cells, we examined the T-cell response to the 13-amino-acid peptide alpha-melanocyte-stimulating hormone (alpha-MSH). To determine the fine specificity of T-cell recognition, T cells specific for alpha-MSH, and genetically restricted by I-Ab/d, were challenged with different alpha-MSH analogs and homologs. It was found that intact alpha-MSH, including the blocked amino and carboxy termini of the native molecule, was required for T-cell responsiveness. Antigen-presenting cells (APC) could be briefly pulsed with alpha-MSH and then present the alpha-MSH antigenic determinant to T cells, indicating that the relevant antigen was retained by the APC. APC stimulatory capacity was dramatically reduced by aldehyde treatment of the APC, or by pulsing the APC with alpha-MSH at low temperature. Efficient alpha-MSH pulsing was also impaired by treatment of the APC with the carboxylic ionophore, monensin, but not by the lysosomotropic agents chloroquine and methylamine. In addition, isolated APC plasma membranes added to the T cells in the presence of soluble alpha-MSH were not stimulatory. However, plasma membranes isolated from APC that had been previously pulsed with alpha-MSH retained stimulatory activity for T-cell responses. The only detectable alpha-MSH contained in these pulsed APC membranes was in an acid-stable complex of higher molecular weight than native peptide. The amount of alpha-MSH detected in the cellular membrane fraction isolated by density gradient sedimentation was also reduced by treatments that reduced the APC stimulatory capacity, such as pulsing at low temperature or in the presence of monensin. Taken together, these results suggest that processing of alpha-MSH is unlike that heretofore described for other peptide antigens and seems to involve APC handling to form the stimulatory moiety presented on the APC surface.
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PMID:Functional and biochemical parameters of peptide antigen presentation. 283 74

Circulating met-enkephalin-like immunoreactivity (MLI) rises in man after chlorpropamide and ethanol although the origin and molecular forms of circulating MLI are not well defined. We have studied the response to oral ethanol in conscious and anaesthetised dogs pretreated with chlorpropamide. In conscious dogs MLI rose from a basal level of 29 +/- 7 pg/ml to a peak of 55 +/- 14 pg/ml 10 min after ethanol (P less than 0.001). In anaesthetised animals, following ethanol, plasma MLI rose in caval (35 +/- 6 pg/ml to a peak of 70 +/- 10 pg/ml), in portal (28 +/- 6 pg/ml to 51 +/- 6 pg/ml) and in adrenal blood (897 +/- 316 pg/ml to 1483 +/- 298 pg/ml; P less than 0.001). Biogel P-4 chromatography of caval and portal basal plasma showed 87% of MLI measured coeluted with the synthetic pentapeptide, while chromatography of peak plasma showed that only 65% coeluted with the pentapeptide and the remaining 35% was of larger molecular size. Sephadex G75 chromatography of adrenal vein plasma revealed three peaks of MLI of differing molecular sizes (8 k = 69.7%; 3-5 k = 12.1% and the pentapeptide = 18.2%). Treatment of the column fractions with trypsin and carboxypeptidase B resulted in the generation of new MLI with peaks of approximate molecular sizes 31 k (10.4%), and 18 k (37.1%) in addition to 8 k (40.0%), 3-5 k (5.0%) and the pentapeptide (7.5%). Acetaldehyde involvement in MLI release was investigated. Following acetaldehyde infusion, plasma MLI rose both in caval (35 +/- 9 pg/ml to 86 +/- 8 pg/ml) and adrenal vein (417 +/- 121 pg/ml to 1768 +/- 433 pg/ml) bloods. Thus we have established an animal model which enables further study of the mechanisms of MLI release and characterisation of the molecular forms. The adrenal medulla, unlike the gut, may be an important source of circulating met-enkephalin and acetaldehyde formation an essential intrinsic component of chlorpropamide-ethanol induced met-enkephalin release.
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PMID:Chlorpropamide-ethanol induced met-enkephalin secretion in dogs: release mechanisms and biochemical characterisation. 666 30

The activity of single neurons in rat cortex or hippocampus (HPC) was recorded to test two hypotheses: (1) neuronal effects of ethanol are mediated by an endogenous opiate-like mechanism (for example, by release of an endogenous opioid peptide), and; (2) ethanol-induced formation of aldehyde-catecholamine condensation products (tetrahydroisoquinolines; TIQs) might contribute to some acute actions of ethanol. Ethanol and all TIQs were applied to single neurons from multibarrel micropipettes by electroosmosis or pressure. Ethanol most often inhibited neurons of the parietal cortex, while activating most HPC pyramidal neurons. Tetrahydropapaveroline (THP) most often inhibited the spontaneous and glutamate- or acetylcholine (ACh)-induced firing of neurons in both these regions, although some excitations were also seen. In contrast, salsolinol and 7-O-methyl-salsolinol predominantly excited HPC pyramidal neurons, but depressed most parietal cortical neurons. Iontophoretic or SC naloxone usually antagonized the excitatory actions of ethanol, salsolinol and methionine5-enkephalin on HPC pyramidal cells; however, ACh-induced speeding also was antagonized occasionally. Conversely, the antimuscarinic agent scopolamine antagonized the excitatory actions of salsolinol, but not those of met-enkephalin, in some HPC pyramidal cells. These results and those of previous studies show that acutely applied ethanol or salsolinol elicits a region-specific pattern of neuronal effects in brain similar to that previously described for opiates: activity is inhibited in several tested brain areas but excited in hippocampus. Furthermore, these excitatory effects are antagonized by naloxone. However, because of the occasional apparent non-specific effects of naloxone and the puzzling antagonism of the salsolinol-induced excitations by scopolamine, some doubt remains whether the opiate-like actions of these substances can be completely attributed to mediation by opiate receptors.
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PMID:Ethanol and some tetrahydroisoquinolines alter the discharge of cortical and hippocampal neurons: relationship to endogenous opioids. 717 89

The Department of Functional Biochemistry was organized at the Institute of Biochemistry of the National Academy of Sciences of Ukraine in 1990. Since that time the collaborators of the Department develop the aldehyde hypothesis of pathogenesis of chronic alcoholism and new high effective methods of its treatment; they have found certain adaptation mechanisms arising in the organism under stress states and pathogenetic mechanisms of formation and development of the radiation encephalopathy in victims of the accident at the Chernobyl NPP. The department researchers have published 92 works.
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PMID:[Interdepartmental division of functional biochemistry]. 757 Oct 68

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

The effects of acute and chronic treatments with ethanol and acute treatments with an ethanol metabolite, acetaldehyde, on proopiomelanocortin (POMC) mRNA expression were compared with those of these agents on the secretion of a POMC gene product, beta-endorphin (beta-EP) peptide. The level of POMC mRNA in cultured cells was determined using an RNase protection assay, and the accumulation of immunoreactive beta-EP (IR-beta-EP) peptide in the culture medium was measured by radioimmunoassay. Treatment of hypothalamic cells with 25-, 50-, and 100-mM doses of ethanol or 12.5 and 25 microM acetaldehyde for 3 h increased POMC mRNA levels. The stimulatory effect of ethanol on POMC mRNA levels lasted for a period of 12 h, although the percentage increase of the ethanol-stimulated mRNA level was gradually reduced over time. Acute treatments with ethanol and acetaldehyde also elevated IR-beta-EP secretion from the cultured neurons for a period of 12 h, and the IR-beta-EP secretory response developed desensitization after 24 h of ethanol incubation. The close association between the ethanol-induced IR-beta-EP secretion and ethanol-regulated POMC mRNA expression suggests that ethanol regulates both secretion and production of beta-EP peptide in the hypothalamic neurons.
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PMID:Comparison of the effects of alcohol and acetaldehyde on proopiomelanocortin mRNA levels and beta-endorphin secretion from hypothalamic neurons in primary cultures. 770 32

The effect of ethanol, acetaldehyde, and salsolinol on hypothalamic beta-endorphin secreting neurons is studied by using rat fetal hypothalamic neurons in primary culture. Exposure of these neuronal cells to different concentrations of ethanol (12.5-50 mM) and acetaldehyde (12.5-50 microM) caused a concentration-dependent increase in the secretion of beta-endorphin. Salsolinol (12.5-50 microM) did not cause any significant change in the secretion of beta-endorphin. Ethanol's effect was short-lasting (2 hr). Acetaldehyde's effect on beta-endorphin secretion was greater and longer lasting, as compared with ethanol. Ethanol and salsolinol do not have any effect on cell viability, whereas higher concentrations of acetaldehyde appear to reduce the number of viable cells after 6 hr of treatment. None of the above treatments has any effect on cellular DNA content. These results suggest that ethanol is a potent stimulator of hypothalamic beta-endorphin. These results also show for the first time that ethanol's metabolite acetaldehyde is more potent in stimulating beta-endorphin secretion and may be significant in the ethanol regulated beta-endorphin secretion.
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PMID:Effect of alcohol, acetaldehyde, and salsolinol on beta-endorphin secretion from the hypothalamic neurons in primary cultures. 811 41

Adenohypophysial cell types and neurohypophysial tissues were investigated in the cobalt variant of the rainbow trout, which possesses an irregularly-shaped pituitary. The pituitary remnant was completely detached from the hypothalamus in all but one fish, in which a remnant was associated with the hypothalamus. Prolactin (PRL) and growth hormone (GH) cells were predominant cell types in all pituitary remnants, forming PRL and GH areas, respectively. There were fewer somatolactin (SL) and melanophore-stimulating hormone cells than in normal fish. There were few corticotropin cells in cobalt and normal trout. Although aldehyde-fuchsin positive cells were also present, positively-staining fibers were not detected in any of remnants examined. Plasma SL levels were much lower in cobalt than in normal trout. Plasma levels of GH and T3 were significantly lower in cobalt than in normal fish. Plasma levels of PRL, T4 and cortisol, plasma osmolality, ions (Na+, K+, Ca2+, and Mg2+), glucose, triglyceride, free fatty acids, and amino nitrogen concentrations were similar in the two groups. Cobalt variants thus lack hypophysial pars intermedia and neurohypophysial tissues. Various abnormalities of the cobalt variant, such as the cobalt blue body color and the fat deposition in the abdominal cavity, may be related to the absence of the pars intermedia.
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PMID:Pituitary of "cobalt" variant of the rainbow trout separated from the hypothalamus lacks most pars intermedial and neurohypophysial tissue. 826 55

Tetrahydroisoquinolines (TIQs) are thought to play an important role in the process of development of alcohol dependence. Being a condensation product between the alcohol metabolite acetaldehyde and dopamine they might be involved in the balance of the opioid system as well as the reward system. Therefore, the influence of the TIQ salsolinol (SAL) on the pro-opiomelanocortin (POMC) gene expression was investigated using the ArT-20 mouse anterior pituitary tumor cell line. Our results show a significant decrease in the POMC gene expression by the S(-)-enantiomer of SAL. The basal secretion of adrenocorticotropin (ACTH) as well as the corticotropin-releasing factor (CRF)-stimulated ACTH released remained unchanged after R(+)- and S(-)-SAL treatment. Interestingly, it was clearly shown that a reduction of intracellular cAMP level occurred after the treatment of the cells with S(-)-SAL whereas R(+)-SAL did not affect the cAMP production. The obtained results suggest that S(-)-SAL is possibly involved in the establishment of the opioid deficiency in alcoholics.
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PMID:Effect of S(-)- and R(+)-salsolinol on the POMC gene expression and ACTH release of an anterior pituitary cell line. 851 40


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