Ethanol and liver protein synthesis in vivo

Summary Ethanol was administered i.p. to adult roosters during hormonally induced vitellogenin synthesis. At moderate doses, ethanol had no influence on the synthesis of vitellogenin nor did it cause alterations in the size distribution of liver polyribosomes.This was supported in part by a grant from the Foundation for Alcohol Studies, Finland.     

Phenobarbital markedly increases liver weight in walker carcinosarcoma bearing rats

Riassunto Gli autori hanno dimostrato che nei ratti portatori di tumore di Walker (carcinosarcoma 256), un trattamento eseguito 48 h prima con phenobarbital produce un aumento del rapporto peso fegato/peso corporeo pari al 26%, mentre esso è soltanto del 6% dei ratti normali. Tale fatto si accompagna ad aumento di contenuto totale di proteine, di RNA e di DNA.     

乙醇燃料改质对HCCI燃烧特性的影响

为研究乙醇经过改质后,改质气浓度和改质气进入气缸相位对乙醇HCCI燃烧特性的影响,以一台改造的实验发动机上为模型,用CHEMKIN4．0软件进行模拟。模拟结果表明,乙醇经过改质后,改质气的主要组分为H2、CO、H2O和OH基;随着改质气浓度的增加,缸内压力升高,燃烧始点提前,缸内最高压力升高;随着改质气进入气缸相位逐渐接近上止点,HCCI燃烧始点逐渐推后,缸内的最高压力出现变化,改质气在上止点前14°CA进入气缸,缸内最高压力减小,改质气在上止点前12°CA进入气缸,缸内压力达到最大,随着改质气进入气缸相位逐渐减小,缸内最高压力逐渐减小。因此,在上止点前12°CA进入气缸是较优的相位。     

Ethanol from cellulose

Summary An excess of organic waste, containing up to 60% cellulose and hemicellulose is produced worldwide. The conversion of this cellulosic material to ethanol is discussed: The two-step process consisting of a hydrolysis step to glucose and the subsequent fermentation by yeasts; and the one-step process, a fermentation of the cellulose by the anaerobic thermophileClostridium thermocellum, or by a thermophilic, anaerobic, defined mixed culture. The use of the latter seems to be very feasible., To achieve an economic process, it is suggested to combine this approach with a thermophilic fermentation of the effluent and/or stillage obtained to produce methane.Acknowledgment. Part of this work was supported by Energy and Research Development Administration contract number EY-76-509-0888-M003, and by the Deutsche Forschungsgemeinschaft.     

Ethanol metabolism inDrosophila melanogaster

Summary A quantitative study of the transformation of ethanol into acetaldehyde shows that, inDrosophila melanogaster, the mitochondrial ethanol oxidizing system is not very active but that the part played by catalase appears more important than expected. For a strain without alcoholdehydrogenase, ethanol is highly toxic. The presence of acetaldehyde in the culture medium is toxic for all the strains studied. But, since even a strain without any aldehydeoxidase lives normally, the metabolic production of acetaldehyde does not seem dangerous.     

Ethanol and opioid receptor signalling

Summary Ethanol may modulate endogenous opioid systems by disrupting opioid receptor signalling. Low concentrations of ethanol slightly potentiate -opioid receptor binding by increasing receptor B_max, and, in some cases, chronic ethanol exposure decreases the density or affinity of the -opioid receptors. By contrast, high concentrations of ethanol acutely decrease -opioid receptor binding by decreasing receptor affinity, whereas chronic exposure of animals and neuronal cell lines to lower concentrations of ethanol leads to possibly adaptive increases in the density or affinity of the -opioid receptors. In the neuronal cell line NG108-15, ethanol does not up-regulate the -opioid receptor by blocking receptor degradation or endocytosis, but protein synthesis is required for this response. Up-regulation of the -opioid receptor renders ethanol-treated NG108-15 cells 3.5-fold more sensitive to opioid inhibition of adenylyl cyclase. Long-term treatment with ethanol also increases maximal opioid inhibition in NG108-15 cells, possibly by decreasing levels of G_s and its mRNA. Ethanol differentially modulates signal transduction proteins in three additional neuronal cell lines, N18TG2, N4TG1, and N1E-115. Ethanol-treated N18TG2 cells show the least up-regulation of the -opioid receptor, little heterologous desensitization of adenylyl cyclase, and no changes in G_s or G_i. By contrast, ethanol-treated N1E-115 cells show the largest up-regulation of the -opioid receptor, the most heterologous desensitization of adenylyl cyclase, and concentration-dependent decreases in G_s and increases in G_i. Further analysis of these related neuronal cell lines may help to identify the molecular elements that endow some, but not all, neuronal cells with the capacity to adapt to ethanol.     

Ethanol and opioid receptor signalling

Ethanol may modulate endogenous opioid systems by disrupting opioid receptor signalling. Low concentrations of ethanol slightly potentiate mu-opioid receptor binding by increasing receptor Bmax, and, in some cases, chronic ethanol exposure decreases the density or affinity of the mu-opioid receptors. By contrast, high concentrations of ethanol acutely decrease delta-opioid receptor binding by decreasing receptor affinity, whereas chronic exposure of animals and neuronal cell lines to lower concentrations of ethanol leads to possibly adaptive increases in the density or affinity of the delta-opioid receptors. In the neuronal cell line NG108-15, ethanol does not up-regulate the delta-opioid receptor by blocking receptor degradation or endocytosis, but protein synthesis is required for this response. Up-regulation of the delta-opioid receptor renders ethanol-treated NG108-15 cells 3.5-fold more sensitive to opioid inhibition of adenylyl cyclase. Long-term treatment with ethanol also increases maximal opioid inhibition in NG108-15 cells, possibly by decreasing levels of G alpha s and its mRNA. Ethanol differentially modulates signal transduction proteins in three additional neuronal cell lines, N18TG2, N4TG1, and N1E-115. Ethanol-treated N18TG2 cells show the least up-regulation of the delta-opioid receptor, little heterologous desensitization of adenylyl cyclase, and no changes in G alpha s or G alpha i. By contrast, ethanol-treated N1E-115 cells show the largest up-regulation of the delta-opioid receptor, the most heterologous desensitization of adenylyl cyclase, and concentration-dependent decreases in G alpha s and increases in G alpha i. Further analysis of these related neuronal cell lines may help to identify the molecular elements that endow some, but not all, neuronal cells with the capacity to adapt to ethanol.     

Ethanol and the benzodiazepine-GABA receptor-ionophore complex

Summary Ethanol has a pharmacological profile similar to that of classes of drugs like benzodiazepines and barbiturates, which enhance GABAergic transmission in the mammalian CNS. Several lines of behavioral, electrophysiological and biochemical studies suggest that ethanol may bring about most of its effects by enhancing GABAergic transmission. Recently, ethanol at relevant pharmacological concentrations has been shown to enhance GABA-induced³⁶Cl-fluxes in cultured spinal cord neurons, synaptoneurosomes and microsacs. These enhancing effects of ethanol were blocked by GABA antagonists. Ro15-4513, an azido analogue of classical BZ antagonist Ro15-1788, reversed most of the behavioral effects of ethanol and other effects involving³⁶Cl-flux studies. The studies summarized below indicate that most of the pharmacological effects of ethanol can be related to its effects on GABAergic transmission.     

Ethanol and the benzodiazepine-GABA receptor-ionophore complex

Ethanol has a pharmacological profile similar to that of classes of drugs like benzodiazepines and barbiturates, which enhance GABAergic transmission in the mammalian CNS. Several lines of behavioral, electrophysiological and biochemical studies suggest that ethanol may bring about most of its effects by enhancing GABAergic transmission. Recently, ethanol at relevant pharmacological concentrations has been shown to enhance GABA-induced 36Cl-fluxes in cultured spinal cord neurons, synaptoneurosomes and microsacs. These enhancing effects of ethanol were blocked by GABA antagonists. Ro15-4513, an azido analogue of classical BZ antagonist Ro15-1788, reversed most of the behavioral effects of ethanol and other effects involving 36Cl-flux studies. The studies summarized below indicate that most of the pharmacological effects of ethanol can be related to its effects on GABAergic transmission.     

Ethanol metabolism in Drosophila melanogaster.

A quantitative study of the transformation of ethanol into acetaldehyde shows that, in Drosophila melanogaster, the mitochondrial ethanol oxidizing system is not very active but that the part played by catalase appears more important than expected. For a strain without alcoholdehydrogenase, ethanol is highly toxic. The presence of acetaldehyde in the culture medium is toxic for all the strains studied. But, since even a strain without any aldehydeoxidase lives normally, the metabolic production of acetaldehyde does not seem dangerous.     

Ethanol diminishes the toxicity of the mushroomAmanita phalloides

Summary Survival of mice after lethal doses of a lyophilizate fromAmanita phalloides (death cap) was markedly increased by single doses of ethanol applied 30 min before or 5 min after the mushroom. Hepatic histopathological damage (confluent necrosis) was largley prevented. Acute, but not chronic, consumption of ethanol may thus influence favorably the outcome of death cap poisoning and should be taken into consideration in the evaluation of therapeutic measures.     

Ethanol inhibition of audiogenic stress induced cardiac hypertrophy

Zusammenfassung Gruppen weiblicher jungfräulicher Albinoratten wurden 2 Wochen lang periodischem Lärm-und Geräuschhintergrund ausgesetzt, während welcher Zeit sie entweder Leitungswasser oder Äthanol trinken durften. Kontrollgruppen wurden bei Abwesenheit des Lärmhintergrunds geprüft. Herzhypertrophie konnte in den Kontrollgruppen mit Äthanol und bei den Ratten (mit Lärmhintergrund) beobachtet werden. Nach Behandlung mit Äthanol war die Herzhypertrophie nicht mehr vorhanden.

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This study was supported by grants from the South Dakota Heart Association and USPHS No. HE-6488. The authors wish to express their appreciation toJ. A. Richardson, P. L. Mayclin andN. L. Burns for invaluable assistance in the technical and construction phases of the present study.     

Ethanol impairs insulin-stimulated mitochondrial function in cerebellar granule neurons

Ethanol impairs insulin-stimulated survival and mitochondrial function in immature proliferating neuronal cells due to marked inhibition of downstream signaling through P13 kinase. The present study demonstrates that, in contrast to immature neuronal cells, the major adverse effect of chronic ethanol exposure (50 mM) in post-mitotic rat cerebellar granule neurons is to inhibit insulin-stimulated mitochondrial function (MTT activity, MitoTracker Red fluorescence, and cytochrome oxidase immunoreactivity). Ethanol-impaired mitochondrial function was associated with increased expression of the p53 and CD95 pro-apoptosis genes, reduced Calcein AM retention (a measure of membrane integrity), increased SYTOX Green and propidium iodide uptake (indices of membrane permeability), and increased oxidant production (dihydrorosamine fluorescence and H2O2 generation). The findings of reduced membrane integrity and mitochondrial function in short-term (24 h) ethanol-exposed neurons indicate that these adverse effects of ethanol can develop rapidly and do not require chronic neurotoxic injury. A role for caspase activation as a mediator of impaired mitochondrial function was demonstrated by the partial rescue observed in cells that were pre-treated with broad-spectrum caspase inhibitors. Finally, we obtained evidence that the inhibitory effects of ethanol on mitochondrial function and membrane integrity were greater in insulin-stimulated compared with nerve growth factor-stimulated cultures. These observations suggest that activation of insulin-independent signaling pathways, or the use of insulin sensitizer agents that enhance insulin signaling may help preserve viability and function in neurons injured by gestational exposure to ethanol.     

Ethanol diminishes the toxicity of the mushroom Amanita phalloides

Survival of mice after lethal doses of a lyophilizate from Amanita phalloides ('death cap') was markedly increased by single doses of ethanol applied 30 min before or 5 min after the mushroom. Hepatic histopathological damage (confluent necrosis) was largely prevented. Acute, but not chronic, consumption of ethanol may thus influence favorably the outcome of death cap poisoning and should be taken into consideration in the evaluation of therapeutic measures.     

Ethanol influence on insulin secretion from isolated rat islets

This study was done to delineate the role of alpha- and beta-adrenergic receptors and cyclic AMP in the mechanism of ethanol effects on insulin release from isolated islets. Rats were given an alpha-adrenergic blocker, phentolamine, or a beta-adrenergic blocker, propranolol. In addition, ethanol 1 g/kg was given intragastrically 1 h prior to sacrifice. Glucose mediated insulin release from isolated islets was enhanced by phentolamine and decreased by propranolol. Ethanol treatment inhibited glucose-induced insulin release from isolated islets of control rats as well as those given phentolamine and/or propranolol. Insulin release from isolated islets in response to dibutyryl-cyclic AMP was attenuated by ethanol. Theophylline enhanced glucose mediated insulin release from control islets but ethanol treatment produced a significant inhibition of insulin response. The data suggest that the site of action of the deleterious effects of ethanol on insulin release from isolated islets in rat does not involve adrenergic system and cyclic AMP.     

Ethanol ingestive behavior as a function of central neurotransmission

Summary Uncontrollable alcohol ingestive behavior has been linked to deficits of central neurotransmission. The pineal gland plays an important role in modulating ethanol intake in numerous animal species. The opioidergic (i.e. -endorphin, enkephalin, and dynorphin) system is involved in both the actions of alcohol and opiates, as well as craving and/or genetic predisposition towards abuse of these two agents. Furthermore, there is significant evidence to link ingestive behaviors with the ventral tegmental accumbens-hypothalamic axis, whereby the biogenic amines dopamine and serotonin are reciprocally involved. Evidence is presented which implicates the striatum and the hypothalamus as possible specific loci for regional differences between alcohol-preferring and alcohol-nonpreferring mice. We believe that photoperiod-induced alcohol ingestive behavior may involve alterations in both pineal and hypothalamic opioid peptides.