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Results for “Ethanol utilization”

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At least 415 records · Page 23Linked to original sources
PubMed2003

The average ethanol content of beer in the U.S. and individual states: estimates for use in aggregate consumption statistics.

OBJECTIVE: The purpose of this study is to describe the variation in the ethanol content of beer and specific categories of beer, and to illustrate the importance of accurate assessment of ethanol conversion factors for the calculation of apparent ethanol consumption from beer at the state and national levels in the U.S. METHOD: Published sources of brand-level ethanol content, national brand share of beer categories and state beer category market shares are utilized to (1) estimate the mean ethanol content of each beer category in the U.S. for 1995 and 2000, (2) calculate per capita apparent consumption of ethanol from beer for 1995 and 2000 and for each state in 2000 and (3) describe trends in ethanol content for specific beer brands during the 1990s. RESULTS: The mean ethanol content of beer in the U.S. is found to increase from 4.33% (by volume) in 1995 to 4.66% in 2000. Using these estimates, per capita ethanol from beer is found to increase from 1.386 gallons in 1995 to 1.468 gallons in 2000. Use of a constant ethanol conversion, however, indicates a decrease. Application of ethanol content estimates to state-level per capita consumption for 2000 changes the relative rankings of 28 states, compared to the use of a constant 4.5% ethanol conversion. CONCLUSIONS: Improved ethanol conversion factor estimates are found to influence both time trends and the cross-sectional ranking of states, suggesting that analyses of both cross-sectional and time series aggregate ethanol consumption data that fail to consider variation in the ethanol content of beer may be biased.

Alcohol Drinking↗
PubMed1989

In vitro adsorption losses of arachidonic acid and calcium ionophore A23187.

Arachidonic acid (AA) is often utilized in in vitro studies to label cellular pools of AA or to elicit cellular responses dependent on eicosanoid production. Because of the hydrophobic nature of AA, organic diluents such as ethanol or dimethyl sulfoxide are utilized in preparing concentrated solutions. The fate of AA when added to aqueous medium is not generally considered because of the dilution of the AA, although some investigators utilize bovine serum albumin (BSA) to solubilize as well as to trap AA and its hydrophobic metabolites. These experiments demonstrate a rapid and progressive decline in AA concentration when added to aqueous media in tissue baths and in glass test tubes. The extent of the decline was greater in the tissue baths than in the test tubes. The calcium ionophore A23187, which is used to stimulate AA metabolism, is also hydrophobic, and its concentration also decreased when added to aqueous media. The decline in the concentration of both AA and A23187 was due to adsorption to the container walls. The presence of 1% BSA in the aqueous solution attenuated and even eliminated the decline in the concentration, indicating binding of the two agents to the protein. However, the presence of BSA in culture medium inhibited the A23187-induced stimulation of AA metabolites in baboon aortic smooth muscle cells. These results underscore the complexities arising from the in vitro use of hydrophobic substances in biological systems.

Adsorption↗
PubMed1986

Brain benzodiazepine binding sites in ethanol dependent and withdrawal states.

The brain benzodiazepine system has been implicated to be important in both the mechanism, and treatment of ethanol related syndromes. In this report evidence is presented which indicates that "peripheral type" benzodiazepine binding sites are probably more relevant than "central type" receptors for the neurochemical consequences of ethanol dependence and withdrawal states. Utilizing radioreceptor binding techniques 20-50% increases in the binding of [3H]RO-5-4864 (a "peripheral type" ligand) to brain membranes derived from rat cerebral cortex, cerebellum and hippocampus are observed in ethanol dependent rats. These increases persist for 3 days after cessation of ethanol. The number of [3H]RO-5-4864 binding sites in cerebellum returns to normal during 4-7 days after ethanol withdrawal. In all brain areas examined no changes were observed in the "central type" benzodiazepine receptor as judged by [3H]-ethyl-Beta-carboline-3-carboxylate, BCCE binding. Scatchard analysis revealed that the number of [3H]RO-5-4864 binding sites is increased in each brain area while the affinity was unchanged.

Animals↗
PubMed1999

Chronic ethanol, oxygen tension and hepatocyte energy metabolism.

Hepatocytes from ethanol-fed animals, isolated from either whole liver or the periportal or perivenous regions of the lobule, exhibited an ethanol-related decrease in energy state only when they were oxygen deficient. This was accompanied by an ethanol-related decrease in hepatocyte viability. Both periportal and perivenous hepatocytes from ethanol-fed rats demonstrated increased respiration. The observations reported here are consistent with an ethanol-induced increase in oxygen utilization which could render the perivenous region of the lobule relatively oxygen deficient in the intact liver. This oxygen deficit may cause the decreases in energy state and cell viability associated with chronic ethanol consumption. Ethanol-associated loss in hepatocyte viability appeared to correlate better with a decrease in energy state than with an increase in the products of oxidative stress. An investigation of the association between viability and cellular malondialdehyde levels revealed no effects of chronic ethanol consumption on MDA levels in hepatocytes that demonstrated ethanol-related decreases in cell viability.

Animals↗
PubMed2006

[Progress on engineered strains for ethanol production].

With the 21 century's coming, the era of cheap oil is coming to the end. There has been an increasing worldwide interest in fuel ethanol. In the last two decades, lots of work has been done to develop strains for ethanol producing. Research progress on metabolic engineering of strains for fuel ethanol production is summarized, including genetically engineered Saccharomyces cerevisiae to utilize starch, pentose and cellulose, Zymomonas mobilis to ferment arabinose and xylose, Escherichia coli and Klebsiella oxytoca to introduce heterogenous ethanol production pathway. The aim of engineering these strains is to obtain an ideal microorganism which can converse the available carbon sources to ethanol rapidly and efficiently with high tolerance to ethanol and to inhibitory components in the cheap materials such as lignocellulose hydrolysate. The importance of fuel ethanol will be a stimulus to develop engineered hardy strains to utilize cheap materials for high ethanol concentration production. Since both Saccharomyces cerevisiae and Zymomonas mobilis are generally regarded as safe (GRAS), genetically engineered Saccharomyces cerevisiae which can utilize raw starch directly and recombinant Zymomonas mobilis which can ferment glucose, arabinose and xylose in the lignocellulose hydrolysate have potential application to industry in the near future.

Biotechnology↗
PubMed2001

The effect of gamma-vinyl-GABA on the consumption of concurrently available oral cocaine and ethanol in the rat.

It has frequently been reported that a high percentage of individuals, identified as either alcohol- or cocaine-dependent, concurrently abuse both drugs. The experiments reported here represent a continuing effort to develop an animal model to predict the effects of a potential pharmacotherapeutic agent on concurrently available oral ethanol and cocaine. These experiments utilized drinkometer circuitry to assess the effects of gamma-vinyl-GABA (GVG), a gamma-aminobutyric acid (GABA) transaminase inhibitor, on the consumption and temporal pattern of responses for orally self-administered ethanol and cocaine. The results of these experiments showed that GVG, at doses of 100, 200 and 300 mg/kg, reduced both ethanol and cocaine consumption in a dose-related manner. When compared to vehicle, GVG at all doses significantly reduced ethanol consumption while consumption of cocaine was significantly reduced only at 300 mg/kg. This is consistent with data showing that GVG reduces consumption of these drugs when administered alone and data showing that GVG is more potent in reducing ethanol-induced compared to cocaine-induced extracellular dopamine in the nucleus accumbens. Analysis of the temporal pattern of drinking across the session suggests that GVG's effects are due to a disruption of the reinforcing properties of ethanol and cocaine rather than a more general reduction in motor behavior. These data suggest that GVG has potential for clinical use in populations that abuse either alcohol or cocaine alone or in combination.

Alcohol Drinking↗
PubMed1993

Effect of Nystatin on the Metabolism of Xylitol and Xylose by Pachysolen tannophilus.

Ethanol production from xylitol by resting cells of Pachysolen tannophilus was increased 40-fold in the presence of nystatin, amphotericin B, and filipin, a group of antifungal agents that alter the permeability of the plasma membrane. Furthermore, these agents had little or no effect on ethanol formation from xylitol or xylose by the cell extract. During xylose metabolism, nystatin caused the intracellular xylitol to leak out into the medium at a 23-fold-faster rate but did not affect overall xylose utilization and CO(2) evolution. These observations explain the rate of xylitol utilization by cell extract being higher than that by whole cells (J. Xu and K. B. Taylor, Appl. Environ. Microbiol. 59:231-235, 1993) as well as the relative inability of P. tannophilus to utilize xylitol to support significant ethanol production and cell growth.

Journal Article↗
PubMed1985

Brain-gut neuropeptides and the limitation of ethanol consumption.

Recent studies have clearly shown powerful control of ingestive behavior by certain peptides known to be present in both brain and gut tissues. These "brain-gut neuropeptides" are thought to constitute endogenous factors responsible for the normal regulation of food intake. This review explores the potential for a role of these peptides in the limitation of ethanol intake, which shares several features with the control of food intake. The putative satiety role of the neuropeptides cholecystokinin and bombesin, and other brain-gut peptides is briefly described. The conclusion that voluntary ethanol intake is partially controlled as a function of the energy ethanol provides, and the rate of its utilization, is illustrated with data from recent studies of rat and hamster ethanol consumption. The possibility of neuropeptide influence on ethanol intake is presented in light of new findings that cholecystokinin and bombesin inhibit ethanol consumption in the rat. If neuropeptides are demonstrated to modulate ethanol intake by eliciting satiety, this information may be useful in the identification and understanding of the endogenous factors which regulate human alcohol intake, and will suggest possible peptide-based therapeutic interventions for control of alcohol abuse and alcoholism.

Alcohol Drinking↗
PubMed2004

Controlled and behaviorally relevant levels of oral ethanol intake in rhesus macaques using a flavorant-fade procedure.

BACKGROUND: Flavorant-fading procedures can initiate and maintain oral ethanol intake in rodents. The present study developed a similar procedure to achieve controlled and behaviorally relevant levels of ethanol intake in monkeys. METHODS: Male rhesus macaques (N = 13) were initially given the opportunity to consume 0.5 g/kg of a 1% (w/v) ethanol plus 4% (w/v) Tang solution in 1-hr limited-access sessions without the requirement of an operant response. Once consumption was stable at a particular concentration (%) and/or amount (g/kg), animals were given access to higher concentrations and/or amounts of ethanol. Animals were tested on a bimanual motor skill (BMS) task 20 and 90 min after consumption to assess behavioral impairment. Blood alcohol levels (BALs) were assessed after a session in which animals had the opportunity to consume up to 3.0 g/kg of 6% (w/v) ethanol. RESULTS: The gradual fading up of higher concentrations and amounts of ethanol resulted in controlled and robust levels (>2.0 g/kg) of ethanol intake in half of the subjects. Increasing the concentration of the sweetener from 4 to 6% (w/v) was effective in initiating consumption in three animals. Two monkeys required the additional step of presenting the increased-sweetener solutions after a meal (postprandial consumption) to initiate significant ethanol intake. Animals were significantly impaired on the BMS task after consumption of 2.0, 2.5, and 3.0 g/kg of ethanol. Individual consumption ranging from 0.8 to 3.0 g/kg of ethanol produced BALs of 18 to 269 mg/dl. CONCLUSIONS: The flavorant-fading procedure was effective in producing behaviorally relevant levels of ethanol consumption in rhesus macaques. This model facilitated a randomized-dose procedure to determine the behavioral effects of 0.5 to 3.0 g/kg of ethanol. This procedure therefore is of significant utility in determining behavioral or physiologic effects of specific doses of consumed ethanol in monkeys.

Administration, Oral↗
PubMed1993

Selective inhibition of antigen-specific T lymphocyte proliferation by acute ethanol exposure: the role of impaired monocyte antigen presentation capacity and mediator production.

Ethanol consumption is associated with impaired immunity. Our data demonstrate that even a single dose of a biologically relevant concentration (25-150 mM) of ethanol can down-regulate antigen-specific T lymphocyte proliferation. In contrast, ethanol augmented mitogen-induced T cell proliferation, suggesting that its inhibitory effect on antigen-specific T cell proliferation was due to its effects on monocytes (m phi s) rather than on T cells. The immunodepressive effects of ethanol on m phi antigen-presenting cell (APC) capacity were manifested whether alcohol treatment was limited to the antigen uptake-processing period only or was present during the entire period of antigen presentation. These inhibitory effects of ethanol were also evident on both the high-antigen-presenting, Fc gamma RI-negative (-31 +/- 17%), and low-antigen-presenting, Fc gamma RI-positive (-42 +/- 15%) m phi subpopulations. Further analysis demonstrated that ethanol inhibits the production of interleukin-1 beta (IL-1 beta) and induces transforming growth factor beta (TGF-beta) and prostaglandin E2 (PGE2), monocyte-derived mediators that can affect T cell proliferation. Ethanol resulted in a dose-dependent down-regulation of secreted and cell-associated IL-1 beta protein as well as IL-1 beta mRNA levels induced by adherence or bacterial stimulation. The causal relationship between decreased m phi IL-1 beta production, elevated TGF-beta levels, and the decreased m phi APC capacity was further substantiated when exogenous IL-1 beta protein or anti-TGF-beta neutralizing antibody prevented the down-regulatory effect of ethanol on antigen-specific T cell proliferation. Utilizing a cyclooxygenase inhibitor, we also demonstrated that the ethanol-induced decrease in m phi APCs is not mediated by enhanced PGE2 production.

Adult↗
PubMedDate not supplied

Ethanol does not affect serotonin receptor binding in rodent brain.

The effects of ethanol on serotonin (5-hydroxytryptamine, 5-HT) receptor binding in rat and mouse brain were determined under in vitro conditions and in mouse brain following seven days of ethanol ingestion. 5-HT1A receptor characteristics were measured utilizing the agonist [3H]8-hydroxy-2-(di-n-propylamino)tetralin ([ 3H]DPAT), and 5HT2 receptor-binding studies utilized the antagonist [3H]ketanserin. At the highest concentration of ethanol tested in vitro (680 mM), there was only 25% inhibition of [3H]DPAT binding in rat and mouse brain and 14% inhibition of [3H]ketanserin binding in rat brain. Effects of an anesthetic concentration of ethanol (100 mM) on agonist binding in the presence and absence of the guanine nucleotide GTP were also evaluated in vitro in mouse brain. In no case did ethanol (100 mM) significantly affect 5-HT1A or 5-HT2 receptor-binding characteristics. When 5-HT receptor characteristics were measured after mice consumed ethanol for seven days, there was no change in either 5-HT1A or 5-HT2 receptor-binding properties in any of the brain areas examined.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

Stabilization of tumor necrosis factor alpha mRNA by chronic ethanol: role of A + U-rich elements and p38 mitogen-activated protein kinase signaling pathway.

Increased expression of tumor necrosis factor alpha (TNFalpha) in response to chronic ethanol has been implicated in the pathogenesis of alcoholic liver disease. However, the molecular mechanisms by which ethanol increases the levels of TNFalpha are not well characterized. Utilizing Kupffer cells isolated from rats fed an ethanol containing diet and a murine macrophage cell line, RAW264.7, exposed to ethanol in culture, we have demonstrated that exposure to chronic ethanol results in an enhanced expression of lipopolysaccharide (LPS)-induced TNFalpha. While chronic ethanol had no effect on the rate of LPS-induced TNFalpha transcription as measured by nuclear run-on experiments, TNFalpha mRNA half-life was increased by chronic ethanol. Chronic ethanol also potentiated the activation of LPS-induced p38 mitogen-activated protein (MAP) kinase in Kupffer cells, as well as in RAW264.7 cells. Specific inhibition of p38 MAP kinase activation by SB203580 in Kupffer cells or by overexpression of dominant negative p38 MAP kinase in RAW264.7 cells blocked ethanol-mediated TNFalpha mRNA stabilization. Furthermore, using chimeric reporter constructs, we have shown that A + U-rich elements in the 3'-untranslated region of TNFalpha mRNA are not sufficient to impart ethanol-mediated stabilization on TNFalpha mRNA.

3' Untranslated Regions↗
PubMed1984

Renal devitalization with ethanol injection in management of patients with advanced hypernephroma.

Transcatheter injection of ethanol into the renal artery was utilized in 11 patients with hypernephromas, clincally staged C or D, in an attempt to produce renal devitalization. Complete disappearance of the tumor neovascularity was achieved in 9 of 11 patients. Renal divitalization with ethanol injection is safer and more effective than the embolizing technique utilized hitherto and should be included in the primary treatment of hypernephroma in selected cases or in conjunction with other procedures to induce chemical nephrectomy.

Adenocarcinoma↗
PubMed1979

Nitration of polypeptides using ethanol in reaction buffers minimizes crosslinking.

High concentrations of ethanol are effective in reducing the intermolecular cross-linking which predominates when the reactions of tetranitromethane with the carboxypeptidase inhibitor from potatoes, a chymotrypsin inhibitor also from potatoes, and insulin are carried out under standard conditions. Including reagents such as ethanol may be of general utility in the preparation of monomeric nitro-derivatives of hydrophobic, low-molecular-weight proteins.

Buffers↗
PubMed2002

Development of a chemiluminescence ethanol sensor based on nanosized ZrO2.

Chemiluminescence was observed on introducing ethanol vapor to the surface of nanosized ZrO2 and this effect could be utilized to design a sensor for trace ethanol detection. The term cataluminescence (CTL) was used to describe this kind of chemiluminescence because the luminescence is generated by the catalytic oxidation of organic vapors on the solid surface. The proposed sensor showed high sensitivity to ethanol at 195 degrees C. The stability of the gas sensor was demonstrated by continuous reaction with ethanol for 100 h. Quantitative analysis was performed at an optimum wavelength of 460 +/- 10 nm. The chemiluminescence intensity was proportional to the concentration of ethanol from 1.6 to 160 microg ml(-1), with a detection limit of 0.6 microg ml(-1) (signal-to-noise ratio = 3:1). The mechanism of the chemiluminescence reaction is discussed and the results show that one of the possible luminescent intermediates is acetaldehyde. The chemiluminescence on nanosized ZrO2 observed in this work demonstrates the possibility of developing new nanomaterials for low-temperature cataluminescence detection.

Journal Article↗
PubMed1998

Ethanol consumption in rats selectively bred for differential saccharin intake.

Rat lines selectively bred for high ethanol consumption consume more saccharin solution than do their low-ethanol-consuming counterparts. The present study utilized the technique of reciprocal selection to examine the reliability of the saccharin/ethanol relationship; specifically, consumption of 1-10% ethanol solution was measured in rats selectively bred for high vs. low saccharin consumption (Occidental HiS and LoS lines). HiS rats consumed more ethanol than did LoS rats. These results support the idea that individual differences in ethanol and saccharin consumption share some common mechanism(s).

Animals↗
PubMed1991

Brain energy consumption in ethanol-treated, Long-Evans rats.

The cerebral metabolic rate of glucose utilization (CMRGlc) was measured in rats fed liquid diets containing ethanol for 8 wk, after removal of ethanol from the diet and after acute ethanol intoxication. Control rats were pair fed the liquid diets containing isoenergetic amounts of dextrin-maltose. Quantitative autogradiography using [6-14C]glucose measured CMRGlc at the level of individual structures. Digital image techniques created stereograms of brain energy consumption from the autoradiographs. These techniques provided information about CMRGlc throughout the brain. Rats given the ethanol liquid diet drank constantly throughout the day and night. Neuropathological examination of brain revealed no abnormalities from ethanol consumption. Acute ethanol administration to control rats produced a decrease in CMRGlc throughout the brain that was most prominent in structures concerning auditory, visual, memory and motor functions. Chronic ethanol consumption did not reduce CMRGlc to the same degree as acute ethanol intoxication; in fact, it affected only a few structures. The removal of ethanol from chronic ethanol-treated rats for a period of 18 h caused CMRGlc to rise above control values throughout the brain. However, there were no seizures or other evidence of brain dysfunction.

Alcohol Drinking↗