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)

To characterize the effect of ethanol on the hypothalamic beta-endorphin-containing neurons, rat fetal hypothalamic neurons were maintained in primary culture, and the secretion of beta-endorphin (beta-EP) was determined after ethanol challenges. Constant exposure to ethanol at doses of 6-50 mM produced a dose-dependent increase in basal secretion of beta-EP from these cultured cells. These doses of ethanol did not produce any significant effect on cell viability, DNA or protein content. The stimulated secretion of beta-EP following constant ethanol exposure is short-lasting. However, intermittent ethanol exposures maintained the ethanol stimulatory action on beta-EP secretion for a longer time. The magnitude of the beta-EP response to 50 mM ethanol is similar to that of the beta-EP response to 56 mM of potassium. Ethanol-stimulated beta-EP secretion required extracellular calcium and was blocked by a calcium channel blocker; a sodium channel blocker did not affect ethanol-stimulated secretion. These results suggest that the neuron culture system is a useful model for studying the cellular mechanisms involved in the ethanol-regulated hypothalamic opioid secretion.
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PMID:Effect of acute ethanol on beta-endorphin secretion from rat fetal hypothalamic neurons in primary cultures. 221 79

Content of Met-enkephalin in striatum and of beta-endorphin in rat hypophysis were estimated after administration of ethanol and alpha-interferon into the animals. Ethanol decreased Met-enkephalin content in striatum and of beta-endorphin in hypophysis. Preadministration of alpha-interferon into brain ventricles before ethanol administration led to an increase in concentration of Met-enkephalin, while content of beta-endorphin was unaltered. In peripheric administration alpha-interferon normalized content of beta-endorphin in adenohypophysis but did not affect the Met-enkephalin concentration. Effects of alpha-interferon on content of Met-enkephalin and beta-endorphin, related to dissimilar organization of the opiate systems in hypophysis and striatum tissues, are discussed.
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PMID:[Modification by alpha-interferon of ethanol-induced changes in the level of opioid peptides in the rat striatum and hypophysis]. 238 36

Activation of the hypothalamic-pituitary-adrenal axis (HPAA) by single-dose ethanol administration, which achieved moderately high blood ethanol levels, was explored in naive rats in order to determine the mechanism of ethanol's activation of the stress axis. Adult male rats received a single dose (3.2 g/kg body weight-1 of a 12% solution of ethanol in physiological saline. The plasma concentration of immunoreactive (ir) adrenocorticotropic hormone (ACTH), beta-endorphin (BE) and corticosterone (CS) was determined by radioimmunoassay, whereas, plasma concentrations of epinephrine (E) and norepinephrine (NE) were quantified following reverse-phase liquid chromatographic separation and amperometric detection. Ethanol induced maximal plasma ACTH levels within minutes, which declined toward basal levels by 60 min, whereas, plasma concentration of CS rose rapidly and remained elevated at 60 min. Plasma ACTH and CS levels in saline-treated control animals did not vary significantly at any time point. Consistent with co-release of ACTH from corticotrophs, the plasma concentration of ir-BE increased 5-fold at 15 min and declined towards basal levels at 60 min after-ethanol challenge. Plasma E increased 10- to 20-fold as compared to saline controls or preinjection levels and returned to preinjection levels by 90 min, in a manner similar to ethanol-induced changes in proopiomelanocortin-derived peptides and CS. Removal of the adrenal medulla and thus the source of E prior to ethanol administration, did not attenuate activation of the HPAA. Passive immunoneutralization of arginine vasopressin (AVP), using a high-titer AVP antiserum and a protocol which was found to block ether-induced ACTH secretion by 40% in adult male rats, failed to even partially block ethanol-induced ACTH or CS secretion. The results of this study indicate that neither adrenal medulla-derived E nor AVP are significant regulators or coregulators of corticotroph secretions following a moderately high, single-dose, intragastric administration of ethanol.
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PMID:Single-dose ethanol administration activates the hypothalamic-pituitary-adrenal axis: exploration of the mechanism of action. 255 77

It was shown, that stress increased the level of ACTH, beta-endorphin and corticosterone in the blood plasma of the rat. Injection of ethanol (1 g/kg) decreased the level of ACTH, but increased the levels of beta-endorphin in the rat subjected to immobilization stress. The immobilization lowered the levels of met-enkephalin in the striatum and medulla oblongata, but increased the content of neuropeptide in the adrenal glands. The concentration of leu-enkephalin and DSIP remained unchanged following the stress. Ethanol reversed the action of immobilization on the level of met-enkephalin in the striatum, but increased the content of DSIP in the thalamus. These results indicate that ethanol modified the activity of pituitary-adrenal-axis during stress and probably the stress-protective action of ethanol partly performed with the involvement of DSIP.
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PMID:[Effects of ethanol on the concentration of neuropeptides, ACTH and corticosterone during immobilization stress]. 255 2

Of three casein phosphatases isolated from the cytosol of human cord blood erythrocytes two were cobalt-dependent, E2 and E3. In the presence of CoCl2, E2 activity was the most prominent. In addition to casein, E2 dephosphorylated phosvitin and p-nitrophenyl phosphate (p-NPP) with pH optima at 6.8-7.2 for proteins and 9.0 for p-NPP. The native enzyme had a molecular weight of 104,000 daltons after AcA-44 Ultrogel filtration. According to SDS/PAGE it consisted of two subunits, 78,000 and 15,000 daltons. The 104,000-dalton form exhibited Michaelis-Menten kinetics and had the greatest affinity for casein between protein substrates tested. Ethanol denaturated the enzyme by 80%. Optimal activation of E2 phosphatase was achieved with 5 mmol/l CoCl2 which did not affect the catalytic properties of the enzyme but did affect the rate of 'E-S' complex formation. Inorganic pyrophosphate was not inhibitory for the 104,000-dalton enzyme. Judging by all these properties the natural substrate for E2 casein phosphatase could be P-pyruvate kinase.
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PMID:Cobalt-dependent protein phosphatases from human cord blood erythrocytes. II. Further characterization of E2 casein phosphatase. 283 85

The stimulatory effect of ethanol on the hypothalamo-pituitary-adrenal (HPA) axis was investigated in the long-sleep (LS) and short-sleep (SS) lines of mice. Plasma corticosterone concentrations peaked 30 min after IP administration of ethanol in both lines of mice. Ethanol produced dose-dependent elevations in plasma corticosterone in both LS and SS mice; however, at low doses of ethanol (0.25 to 1 g/kg) the adrenocortical response observed in LS mice was markedly greater than in SS mice. Passive immunoneutralization of circulating corticotropin releasing factor (CRF) completely abolished ethanol-induced elevation in plasma corticosterone in LS mice. CRF or ACTH (adrenocorticotropin) produced dose-dependent elevations in plasma corticosterone in the two lines of mice. Epinephrine co-administered with CRF did not potentiate the adrenocortical response obtained with CRF in either line of mice, and hexamethonium only slightly attenuated ethanol-induced elevations in plasma corticosterone in both lines of mice, suggesting that differentially elevated plasma catecholamines are not responsible for differences in ethanol-induced adrenocortical response. The results suggest that differential adrenocortical response to ethanol exhibited by LS and SS mice is due primarily to differential ethanol-induced CRF release.
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PMID:Ethanol differentially enhances adrenocortical response in LS and SS mice. 285 96

Animals exposed continuously for 14 days to ethanol vapor in an inhalation chamber at sufficient ethanol vapor concentration to maintain blood ethanol levels from 100-250 mg/100 ml exhibited approximately 36% lower corticotropin-releasing factor binding and 24% lower adenylate cyclase activity in anterior (AL) and neurointermediate lobe (NIL) membranes of the pituitary gland compared to controls not treated with ethanol. To determine the effect of chronic ethanol exposure on proopiomelanocortin (POMC) biosynthesis, the levels of POMC mRNA in the AL and NIL were quantified by Northern blot and slot blot techniques. Ethanol treatment for 1, 7, or 14 days produced a time-related decrease in POMC mRNA levels, relative to total RNA levels, in both the AL and NIL. Ethanol treatment caused a greater reduction in NIL POMC mRNA than in AL POMC mRNA. Exposure to ethanol vapors for 14 days decreased immunoreactive beta-endorphin in plasma by approximately 82%. The observed reduction of immunoreactive beta-endorphin in plasma after long term exposure of rats to ethanol may be related to the alcohol-mediated decrease in corticotropin-releasing factor binding and adenylate cyclase activity, which, in turn, leads to decreased intracellular POMC levels through reduced production of POMC mRNA in the AL and NIL of the rat pituitary gland.
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PMID:Ethanol exposure decreases pituitary corticotropin-releasing factor binding, adenylate cyclase activity, proopiomelanocortin biosynthesis, and plasma beta-endorphin levels in the rat. 293 42

beta-Endorphin-like immunoreactivity (BE-LI) was measured in 7 brain regions of Swiss-Webster mice after 24, 48 and 72 h of exposure to ethanol vapor following a priming injection of ethanol and daily injections of pyrazole HCl to inhibit ethanol metabolism. Control mice in identical chambers received pyrazole injections but breathed air only. Ethanol dependence was confirmed by scoring additional groups of mice for handling-induced convulsions during withdrawal after each exposure duration. Measurement of anterior and neurointermediate (NIL) pituitary BE-LI, alpha-MSH and ACTH and plasma corticosterone confirmed earlier results showing NIL depletion of all 3 peptides at 24 h and increased plasma corticosterone concentrations at 72 h in ethanol-exposed mice. In brain extracts from ethanol-dependent mice, BE-LI was significantly reduced in the hypothalamus and midbrain with the greatest reduction occurring at 24 h. In forebrain, cerebral cortex, septum and hippocampus, pyrazole treatment significantly reduced BE-LI relative to an unhandled control group, and ethanol exposure tended to reverse this effect. HPLC of hypothalamic extracts revealed no differences in proportions of molecular forms of beta-endorphin-like peptides between 24 h control and ethanol-exposed groups. The predominant BE-LI peak in both groups co-eluted with opiate-active unmodified beta-endorphin. Ethanol dependence in mice is associated with regionally selective decreases in brain beta-endorphin concentration.
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PMID:Influence of ethanol dependence on regional brain content of beta-endorphin in the mouse. 294 58

Ethanol administration has been shown to affect beta-endorphin (beta-E) levels in most brain areas. Chronic ethanol treatment has also lead to changes in the levels of Met- and Leu-enkephalin which may be due to recent finding that enkephalin A activity is significantly altered. To determine if proteolytic enzymes responsible for beta-E metabolism at the pSPM are also altered, we studied the effect of chronic ethanol (7% v/v; 8 days) administration on in vitro central beta-E metabolism in male C57/BL mice. Purified SPM was time-course incubated with beta-E (20 microM) for 30-120 min and subjected to HPLC analyses for determination of beta-endorphin and related fragments. Chronic ethanol significantly reduced the half-life for beta-E at the pSPM (T1/2 = 50/min) versus controls (T1/2 = 100.4 min). Chronic ethanol also caused significant accumulation of the behaviorally active alpha- and gamma-type endorphins formed at the pSPM. These results suggest that chronic ethanol treatment leads to an increase in the activity of peptidases responsible for beta-E metabolism at pSPM leading to an increased formation of both alpha- and gamma-type endorphins which may affect alcohol related behaviors.
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PMID:Ethanol treatment alters beta-endorphin metabolism by purified synaptosomal plasma membranes. 295 86

The possibility was investigated that ethanol, chronically administered, might produce changes in the opioid receptors located on the sympathetic nerves of the rat vas deferens. Administration of ethanol, 3-9 g/kg per day for six days, resulted in tolerance to the hypnotic effects induced by ethanol (4 g/kg i.p.) and pentobarbital (35 mg/kg i.p.). Ethanol administration also resulted in tolerance to the effects of morphine and beta-endorphin on the muscular twitch evoked in the rat vas deferens by neuronal stimulation. In contrast, chronic ethanol did not significantly change the effects on vas deferens contractions induced by exogenous bioamines such as noradrenaline and dopamine and by acetylcholine. These results suggest that ethanol and opioids have certain biochemical mechanisms in common which might express themselves at the level of prejunctional components involved in the modulation of neurotransmitter action in the rat vas deferens.
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PMID:Chronic ethanol administration induces tolerance to morphine and to beta-endorphin responses in the rat vas deferens. 613 27


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