JOURNAL OF FOOD PROCESS ENGINEERING, Issue 5 2009
DANIEL FRANCO
ABSTRACT Oil extraction from Gevuina avellana Mol. (Chilean hazelnut) with ethanol, near the conditions of its azeotrope with water, was carried out in this work. The effects of solubility, liquid-to-solid ratio and moisture content of ethanol were studied using 92% ethanol, azeotropic (96%) and absolute ethanol (99.9%) as solvents. Water content had a high effect on oil solubility, which reached 140 g/L in 99.9% ethanol, whereas it was 40 g/L with azeotropic ethanol. Oil accounted for 93% of total extractable compounds with absolute ethanol. Kinetics studies of the extraction process were performed at 50C, giving as a result apparent diffusivity values near 10,11 m2/s, being the highest values obtained for ethanol 92% (7.5,16 × 10,11). It was also found that the higher the liquid-to-solid ratio, the higher the diffusivity. Simulation of four-stage countercurrent extraction with azeotropic ethanol yielded 23.5% oil extraction, whereas simulation of four-stage cross-flow extraction yielded 40.7%. Ethanol can be an alternative to batch cold pressing or hexane solvent extraction, for G. savellana seeds or meal processing. PRACTICAL APPLICATIONS The results presented in this paper are applicable for obtaining oil from oilseeds by extraction with ethanol. It includes relevant results for the optimization of extraction conditions and particularly those regarding liquid-to-solid ratio and percentage of water. Considering the more specific focus of this research, the results are applicable to obtaining Gevuina avellana oil by using an ethanol-based process, which will allow to avoid one of the cold-pressing process drawbacks: the high oil content of the meal, which is a factor limiting its lifetime. [source]

BRIEF EXPOSURE TO ETHANOL AUGMENTS VASCULAR CONTRACTILITY IN HUMAN CHORIONIC PLATE ARTERIES

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004
Eun Hui Hong
Summary 1.,Heavy alcohol consumption has been known as a risk factor for hypertension, although the mechanism by which alcohol intake causes hypertension remains elusive. 2.,We tested the hypothesis that brief exposure to ethanol augments vascular contractility through the stress response in human chorionic plate arteries. 3.,Human chorionic plate arteries were mounted in organ baths and exposed to 5% ethanol for 15, 30 or 45 min. 4.,Brief exposure for 45 min, but not 15 min, not only augmented contractility to KCl and 5-hydroxytryptamine 5 h after the end of exposure, but also increased the expression of heat shock protein (HSP) 70 in the tissues. 5.,Reverse transcription,polymerase chain reaction showed gradual increases of hsp70 mRNA expression, but not heat shock cognate 70 (hsc70), hsp90, or glucose regulatory protein 78 (grp78) mRNA expression, in an exposure time-dependent manner 3 h after the end of exposure. 6.,These results indicate that ethanol augments vascular contractility through the stress response. [source]

Bioethanol from agricultural waste residues

ENVIRONMENTAL PROGRESS & SUSTAINABLE ENERGY, Issue 1 2008
Pascale Champagne
Abstract Under the Kyoto Protocol, the Government of Canada has committed to reducing its greenhouse gas emissions by 6% from 1990 levels between 2008 and 2012. Ethanol-blended gasolines have the potential to contribute significantly to these emission reductions. Ethanol is derived from biologically renewable resources and can be employed to replace octane enhancers and aromatic hydrocarbons or oxygenates. To date, the ethanol production industry in Canada is comprised mainly of small-scale plants producing ethanol primarily from agricultural crops as feedstock. Research interests in the area of bioethanol production from organic waste materials emerged in the late 1980. Significant advances in lignocellulosic material extraction and enzymatic hydrolysis have been reported in the last decade, however, continued research efforts are essential for the development of technically feasible and economically viable large-scale enzyme-based biomass-to-ethanol conversion processes. This research aims to develop and test an enzyme-based biomass-to-ethanol conversion process, which employs organic waste materials, such as livestock manures, as alternative sources of cellulosic material feedstock. The source of the livestock manure, manure management practices and cellulose extraction procedures have a significant impact on the quantity and quality of the cellulosic materials derived. As such, raw feedstock materials must be carefully characterized to assess the impact of these factors on the yield of bioethanol and residual end products. The success of cellulose-to-ethanol conversion processes for cellulose extracted from these waste materials as feedstock is generally a function of cellulose fiber pretreatment, enzyme selection and operating conditions. These will differ depending on the source of the waste material feedstock. The long-term benefits of this research will be to introduce a sustainable solid waste management strategy for a number of livestock manure and other lignocellulosic waste materials; contribute to the mitigation in greenhouse gases through sustained carbon and nutrient recycling; reduce the potential for water, air, and soil contamination associated with land disposal of organic waste materials; and to broaden the feedstock source of raw materials for the ethanol production industry. © 2007 American Institute of Chemical Engineers Environ Prog, 2008 [source]

Experimental study of flue gas desulfurization using landfill leachate

ENVIRONMENTAL PROGRESS & SUSTAINABLE ENERGY, Issue 1 2007
Ding Sang-lan
Abstract Because of the complexity of landfill leachate's composition, the reaction mechanism of SO2 in flue gas with landfill leachate was studied. The experimental results indicated that the factors influencing SO2 absorption efficiency using landfill leachate as the scrubbing medium were, in decreasing order of importance, pH, Fe2+, Mn2+, and Cl, as catalysts and the concentration of toluene and ethanol. Experiments showed that the pH of landfill leachate was the key factor governing both SO2 absorption and ammonia stripping. With the initial pH of 8.5, the terminal pH 6.0 and L/G ratio 3 L/m3, experimental results showed that average absorption efficiency of SO2 and the stripping efficiency of ammonia were 85 and 44%, respectively. The use of catalysts such as Fe2+ and Mn2+ was important for SO2 absorption when the pH value was below 7.0. The catalytic activity of Mn2+ was greater than that of Fe2+ although the reaction steps were very similar. Ethanol inhibits HSO3,/SO32, oxidation. The HSO3,/SO32, oxidation process improves the solubility of organics such as toluene in the leachate. The solute products of organics were water-soluble and biodegradable and could be used as substrates for bacteria in the post biotreatment. The factorial experiment results showed the effect of Cl,, Fe2+, and Mn2+ as catalysts on the HSO3,/SO32, oxidation has a greater positive impact than ethanol's inhibitory effect on the HSO3,/SO32, oxidation. © 2006 American Institute of Chemical Engineers Environ Prog 26:25,32, 2007 [source]

Separation and aquatic toxicity of enantiomers of the pyrethroid insecticide lambda-cyhalothrin,

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 1 2008
Chao Xu
Abstract Chiral pollutants are receiving growing environmental concern due to differential biological activities of their enantio-mers. In the present study, enantiomeric separation of the pyrethroid insecticide lambda-cyhalothrin (LCT) was investigated by high-performance liquid chromatography (HPLC) using the columns of Chiralpak AD (amylase tris[3,5-dimethyl-phenylcarbamate]), Chiralpak AS (amylase tris[(S)-1-phenyl carbamate]), Chiralcel OD (cellulose tris[3,5-dimethylphenyl carbamate]), and Chiralcel OJ (cellulose tris[4-methyl benzoate]) with different chiral stationary phases. The differential toxicities of the enantiomers in aquatic systems were evaluated using the acute zebrafish (Danio rerio) toxicity test and the zebrafish embryo test. The enantiomers of LCT were separated completely on all the columns tested and detected by circular dichroism at 236 nm. Better separations were achieved at lower temperatures (e.g., 20°C) and lower levels of polar modifiers (,5%) in mobile phase. Ethanol was found to be a good modifier of the mobile phase for all the columns, although isopropanol acted better for the Chiralcel OD column. The (,)-enantiomer was >162 times more toxic than its antipode to zebrafish in the acute test. The embryo test indicated that the exposure to LCT enantioselectively induced crooked body, yolk sac edema, and pericardial edema and that the (,)-enantiomer was 7.2 times stronger than the (+)-enantiomer in 96-h mortality. The malformations were induced by the racemate and its (,)-enantiomer at lower concentrations tested (e.g., 50 ,g L,1), whereas the (+)-enantiomer induced malformations at relatively higher concentrations (,100 ,g L,1). These results suggest that the toxicological effects of chiral pesticides must be evaluated using their individual enantiomers. [source]

Influence of Genetically Predisposed Diabetes on Ethanol-Induced Depression of Cardiac Contraction in Adult Rat Ventricular Myocytes

EXPERIMENTAL PHYSIOLOGY, Issue 3 2002
Jun Ren
Diabetes mellitus and alcohol (ethanol) intake are two positively correlated major risk factors for cardiovascular abnormalities. However, the interaction of the two on cardiac function is largely unknown. The purpose of the present study was to examine the impact of genetically predisposed diabetes on acute ethanol exposure-induced cardiac contractile depression at the myocyte level. Ventricular myocytes from spontaneously biobreeding diabetes-prone (BBDP) rats and their diabetes-resistant littermates (BBDR) were stimulated to contract at 0.5 Hz. Contractile properties analysed include: peak shortening amplitude (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocities of shortening/relengthening (± dL/dt). BBDP rats displayed hyperglycaemia, reduced body weight gain and increased cardiac, hepatic and renal size. Myocytes isolated from BBDP rat hearts exhibited prolonged TPS and TR90 associated with normal PS and ± dL/dt, compared with myocytes from the BBDR group. Acute ethanol exposure (80-640 mg dl,1) caused a concentration-dependent inhibition of PS in both BBDR and BBDP myocytes. However, the degree of inhibition of PS was significantly reduced in BBDP myocytes compared to that of BBDR myocytes. The maximal inhibition was 52.9% and 28.4% in BBDR and BBDP groups, respectively. Ethanol significantly depressed ± dL/dt in both BBDR and BBDP myocytes. In addition, ethanol did not affect TPS or TR90 in either the BBDR or BBDP group. Collectively, these results suggest that the ethanol-induced depression in cardiac myocyte contraction may be ,shadowed' by genetically predisposed diabetes. [source]

Liquid,vapour partition of ethanol in bakery products

FLAVOUR AND FRAGRANCE JOURNAL, Issue 1 2006
Paola Pittia
Abstract Ethanol is a common ingredient in formulated foods, naturally present or added in liquid form in order to achieve the desired sensorial properties. In many complex foods this volatile compound could also serve interesting technological functions, as well as extending their shelf-lives, owing to its capacity to inhibit or reduce the rate of microbial growth. At the European level there are no known restrictions regarding the use of ethanol in foods as a preservative, while in Italy, current regulations allow its addition as an anti-moulding agent in pre-packed bread, at a maximum concentration of 2% on a dry weight basis. This research studied the effect of water activity (aw) and water content on the ethanol vapour pressure of sliced white bread, previously equilibrated at various aw values and with 2% ethanol added. Different aw values were obtained by both rehydration from previously freeze-dried bread, and dehydration from the fresh product. The results showed that both aw and moisture affected the vapour pressure of ethanol as a consequence of water,solute and ethanol,solute interactions in the matrix. These interactions varied according to the modality of equilibration (desorption or absorption) at a given aw. The results are discussed in terms of ethanol activity (ae), computed as the ratio between the ethanol vapour pressure in bread and the vapour pressure of pure ethanol at the same temperature. This index, analogous to aw, proved to be useful in evaluating the ,freedom' of the ethanol present in a food matrix to be released in the vapour phase. Copyright © 2006 John Wiley & Sons, Ltd. [source]

Ethanol and Acetaldehyde Adsorption on a Carbon-Supported Pt Catalyst: A Comparative DEMS Study

FUEL CELLS, Issue 1-2 2004
H. Wang
Abstract The adsorption of ethanol and acetaldehyde on carbon Vulcan supported Pt fuel cell catalyst and the electrochemical desorption of the adsorption products were studied, using electrochemical measurements and differential electrochemical mass spectrosmetry (DEMS), under continuous flow conditions. Faradaic current adsorption transients at different constant adsorption potentials, which also include CO adsorption for comparison, show pronounced effects of the adsorption potential and the nature of the reactant molecule. Acetaldehyde adsorption is much faster than ethanol adsorption at all potentials. Pronounced Had induced blocking effects for ethanol adsorption are observed at very cathodic adsorption potentials, < 0.16,V, while for acetaldehyde adsorption this effect is much less significant. Comparison of the adsorption charge for CO adsorption with the H-upd charge allows differentiation between H-displacement and double-layer charging effects. Continuous bulk oxidation is observed for both reactants at potentials > 0.31,V; for acetaldehyde adsorption, increasing bulk reduction is found at low potentials. Based on the electron yield per CO2 molecule formed and on the similarity with the CO stripping characteristics the dominant stable adsorbate is CO, coadsorbed with smaller amounts of (partly oxidized) hydrocarbon decomposition fragments, which are also oxidized at higher potentials (> 0.85,V) and which can be reductively desorbed as methane or, to a very small extent, as ethane. The presence of small amounts of adsorbed C2 species and the oxidative dissociation of these species in the main CO oxidation potential range is clearly demonstrated by increased methane desorption after a potential shift to 0.85,V. The data demonstrate that the Pt/Vulcan catalyst is very reactive for C-C bond breaking upon adsorption of these reactants. [source]

Electro-Oxidation of Methanol and Ethanol on Poly(3,4-Ethylenedioxythiophene) with Dispersed Pt, Pt + Sn, and Pt + Pb Particles,

FUEL CELLS, Issue 1-2 2003
S. Biallozor
Abstract The influence of tin and lead additives on the catalytic activity of platinum particles dispersed on a poly(3,4-dioxyethylenethiophene) (PEDT) layer deposited on gold or steel towards anodic oxidation of methanol and ethanol was studied. It was found that these additives increase the rate of anodic oxidation of both alcohols. It was also found that the electro-catalytic properties of PEDT depend on the kind of support used for its deposition. The authors have shown that these additives (Pb and Sn) increase the rate of anodic oxidation of both alcohols on platinum deposited on PEDT, but tin was evidently more effective than lead. In the presence of Sn, the steady-state current density of methanol oxidation increases about 100 times, while Pb only promotes the platinum catalyst activity by about 2 times. In the authors opinion the most probable mechanism for the tin promotion effect seems to be a homogenous catalytic reaction with the participation of the Sn (IV) and Sn (II) ions as mediators. [source]

Effects of venlafaxine on ethanol withdrawal syndrome in rats

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2004
Esra Sa
Abstract The present study was designed to investigate the effects of venlafaxine, a serotonin and noradrenaline reuptake inhibitor (SNRI), on ethanol withdrawal syndrome in rats. Adult male Wistar rats (187,319 g) were used for the study. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair-fed an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Venlafaxine (5, 10, 20 and 40 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After the 2nd, 4th and 6th hour of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behaviour and wet dog shakes were recorded or rated. A second series of injections was given at the 6th hour after the first one, and rats were then tested for audiogenic seizures. Venlafaxine produced some inhibitory effects on locomotor hyperactivity, stereotypic behaviours and wet dog shakes. However, a two-way anova of the data did not indicate any significant effect. It reduced the incidence of the audiogenic seizures at the 6th hour of ethanol withdrawal. Venlafaxine (20 mg/kg) also prolonged the latency of the seizures significantly. Our results suggest that acute venlafaxine treatment has limited beneficial effects on ethanol withdrawal syndrome in rats. [source]

Blood pressure and vascular reactivity to endothelin-1, phenylephrine, serotonin, KCl and acetylcholine following chronic alcohol consumption in vitro

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2001
Tijen Utkan
Ethanol has been reported to cause hypertension, the mechanism of which is unknown. Therefore, the effect of chronic ethanol consumption on vascular responsiveness and blood pressure was investigated. Systolic blood pressure was recorded weekly by tail-cuff method. Aortic rings from rats fed chow ad libitum or pair-fed liquid diets containing either ethanol (7.2% v/v) or isocaloric carbohydrate for 4 weeks were placed in organ chambers for isometric tension measurement. There was a mild but significant elevation of the systolic blood pressure in the alcohol-fed rats by week 1 compared to baseline measurements and this remained higher. No significant changes in reactivity of rat isolated aortas to phenylephrine, serotonin, endothelin-1 (ET-1) and KCl were seen in chronic ethanol consumption. In addition, the sensitivity (i.e. pD2) of alcohol-fed aortic rings to the vasoconstrictors was also unchanged compared to controls. Chronic ethanol consumption, however, increased relaxation to acetylcholine with increased pD2 values, but did not alter relaxation to sodium nitroprusside, a cyclic guanosine monophosphate (cGMP)-dependent direct smooth muscle dilator. The results indicate that chronic ethanol consumption significantly potentiates endothelium-dependent relaxations in aortic rings, probably through interference with the production and/or the release of nitric oxide (NO) or adaptive alterations in muscarinic receptors on the endothelial cells, and that increased vascular responsiveness to several vasoconstrictors is not a mechanism responsible for the blood pressure elevation in the chronic alcohol consumption in rats. [source]

Contribution of N2O to the greenhouse gas balance of first-generation biofuels

GLOBAL CHANGE BIOLOGY, Issue 1 2009
EDWARD M. W. SMEETS
Abstract In this study, we analyze the impact of fertilizer- and manure-induced N2O emissions due to energy crop production on the reduction of greenhouse gas (GHG) emissions when conventional transportation fuels are replaced by first-generation biofuels (also taking account of other GHG emissions during the entire life cycle). We calculate the nitrous oxide (N2O) emissions by applying a statistical model that uses spatial data on climate and soil. For the land use that is assumed to be replaced by energy crop production (the ,reference land-use system'), we explore a variety of options, the most important of which are cropland for food production, grassland, and natural vegetation. Calculations are also done in the case that emissions due to energy crop production are fully additional and thus no reference is considered. The results are combined with data on other emissions due to biofuels production that are derived from existing studies, resulting in total GHG emission reduction potentials for major biofuels compared with conventional fuels. The results show that N2O emissions can have an important impact on the overall GHG balance of biofuels, though there are large uncertainties. The most important ones are those in the statistical model and the GHG emissions not related to land use. Ethanol produced from sugar cane and sugar beet are relatively robust GHG savers: these biofuels change the GHG emissions by ,103% to ,60% (sugar cane) and ,58% to ,17% (sugar beet), compared with conventional transportation fuels and depending on the reference land-use system that is considered. The use of diesel from palm fruit also results in a relatively constant and substantial change of the GHG emissions by ,75% to ,39%. For corn and wheat ethanol, the figures are ,38% to 11% and ,107% to 53%, respectively. Rapeseed diesel changes the GHG emissions by ,81% to 72% and soybean diesel by ,111% to 44%. Optimized crop management, which involves the use of state-of-the-art agricultural technologies combined with an optimized fertilization regime and the use of nitrification inhibitors, can reduce N2O emissions substantially and change the GHG emissions by up to ,135 percent points (pp) compared with conventional management. However, the uncertainties in the statistical N2O emission model and in the data on non-land-use GHG emissions due to biofuels production are large; they can change the GHG emission reduction by between ,152 and 87 pp. [source]

Selective mitochondrial glutathione depletion by ethanol enhances acetaminophen toxicity in rat liver

HEPATOLOGY, Issue 2 2002
Ping Zhao
Chronic alcohol consumption may potentiate acetaminophen (APAP) hepatotoxicity through enhanced formation of N -acetyl- p -benzoquinone imine (NAPQI) via induction of cytochrome P450 2E1 (CYP2E1). However, CYP2E1 induction appears to be insufficient to explain the claimed magnitude of the interaction. We assessed the role of selective depletion of liver mitochondrial glutathione (GSH) by chronic ethanol. Rats were fed the Lieber-DeCarli diet for 10 days or 6 weeks. APAP toxicity in liver slices (% glutathione- S -transferase , released to the medium, GST release) and NAPQI toxicity in isolated liver mitochondria (succinate dehydrogenase inactivation, SDH) from these rats were compared with pair-fed controls. Ethanol induced CYP2E1 in both the 10-day and 6-week groups by ,2-fold. APAP toxicity in liver slices was higher in the 6-week ethanol group than the 10-day ethanol group. Partial inhibition of NAPQI formation by CYP2E1 inhibitor diethyldithiocarbamate to that of pair-fed controls abolished APAP toxicity in the 10-day ethanol group only. Ethanol selectively depleted liver mitochondrial GSH only in the 6-week group (by 52%) without altering cytosolic GSH. Significantly greater GSH loss and APAP covalent binding were observed in liver slice mitochondria of the 6-week ethanol group. Isolated mitochondria of the 6-week ethanol group were ,50% more susceptible to NAPQI (25-165 ,mol/L) induced SDH inactivation. This increased susceptibility was reproduced in pair-fed control mitochondria pretreated with diethylmaleate. In conclusion, 10-day ethanol feeding enhances APAP toxicity through CYP2E1 induction, whereas 6-week ethanol feeding potentiates APAP hepatotoxicity by inducing CYP2E1 and selectively depleting mitochondrial GSH. [source]

Alcohol-induced free radicals in mice: Direct toxicants or signaling molecules?

HEPATOLOGY, Issue 5 2001
Ming Yin
Tumor necrosis factor , (TNF-,) and free radicals are produced in early alcohol-induced liver injury. Recently, pathology caused by alcohol was blocked nearly completely in tumor necrosis factor , receptor 1 (TNF-R1) knockout mice. With this model, it is now possible to evaluate whether free radicals are directly toxic or act as redox regulators of TNF-, production. Specifically, if free radicals were directly toxic, a parallel decrease in free radicals and pathology in TNF-R1 knockout mice would be predicted. If they only affect TNF-, production, radicals would be expected to remain high while pathology is diminished. Accordingly, free radical production in TNF-R1 knockout mice was studied here. The enteral alcohol delivery model used mice lacking TNF-R1 (p55) and wild-type control C57Bl/6J mice. Animals received a liquid diet continuously with either ethanol or isocaloric maltose-dextrin as control for 4 weeks. Urine ethanol levels fluctuated from 10 to 500 mg/dL in a cyclic pattern in mice receiving ethanol. Ethanol elevated liver:body weight ratios, serum alanine transaminase (ALT) levels, and pathology scores in wild-type mice. These parameters were blunted nearly completely in TNF-R1 knockout mice. Ethanol treatment increased free radical production in wild-type mice compared with animals fed a high-fat control diet. There were no differences in intensity of free radical signals regardless of the presence or absence of TNF-R1; however, pathology differed markedly between these groups. These findings are consistent with the hypothesis that free radicals act as redox signals for TNF-, production and do not directly damage cells in early alcohol-induced hepatic injury. [source]

Chronic ethanol increases adeno-associated viral transgene expression in rat liver via oxidant and NF,B-dependent mechanisms

HEPATOLOGY, Issue 5 2000
Michael D. Wheeler
Recombinant adeno-associated virus (rAAV) transduction is limited in vivo, yet can be enhanced by hydroxyurea, ultraviolet-irradiation, or adenovirus coinfection, possibly via mechanisms involving stress in the host cell. Because chronic ethanol induces oxidative stress, it was hypothesized that chronic ethanol would increase rAAV transduction in vivo. To test this hypothesis, rAAV encoding ,-galactosidase was given to Wistar rats that later received either ethanol diet or high-fat control diet via an enteral-feeding protocol for 3 weeks. Expression and activity of ,-galactosidase in the liver were increased nearly 5-fold by ethanol. The increase in transgene expression was inhibited by antioxidant diphenylene iodonium (DPI), which is consistent with the hypothesis that ethanol causes an increase in rAAV transduction via oxidative stress. Ethanol increased DNA synthesis only slightly; however, it increased the nuclear transcription factor ,B (NF,B) 4-fold, a phenomenon also sensitive to DPI. Moreover, a 6-fold increase in rAAV transgene expression was observed in an acute ischemia-reperfusion model of oxidative stress. Transgene expression was transiently increased 24 hours after ischemia-reperfusion 3 days and 3 weeks after rAAV infection. Further, adenoviral expression of superoxide dismutase or I,B, superrepressor inhibited rAAV transgene expression caused by ischemia-reperfusion. Therefore, it is concluded that ethanol increases rAAV transgene expression via mechanisms dependent on oxidative stress, and NF,B likely through enhancement of cytomegaloviral (CMV) promoter elements. Alcoholic liver disease is an attractive target for gene therapy because consumption of ethanol could theoretically increase expression of therapeutic genes (e.g., superoxide dismutase). Moreover, this study has important implications for rAAV gene therapy and potential enhancement and regulation of transgene expression in liver. [source]

Estrogen is involved in early alcohol-induced liver injury in a rat enteral feeding model

HEPATOLOGY, Issue 1 2000
Ming Yin
The aim of this study was to investigate whether reduction in blood estrogen by removal of the ovaries would decrease the sensitivity of female rats to early alcohol-induced liver injury using an enteral ethanol feeding model, and if so, whether estrogen replacement would compensate. Livers from ovariectomized rats with or without estrogen replacement after 4 weeks of continuous ethanol exposure were compared with nonovariectomized rats in the presence or absence of ethanol. Ethanol increased serum alanine transaminase (ALT) levels from 30 ± 6 to 64 ± 7 U/L. This effect was blocked by ovariectomy (31 ± 7) and totally reversed by estrogen replacement (110 ± 23). Ethanol increased liver weight and fat accumulation, an effect that was minimized by ovariectomy and reversed partially by estrogen replacement. Infiltrating leukocytes were increased 6.7-fold by ethanol, an effect that was blunted significantly by ovariectomy and reversed by estrogen replacement. Likewise, a similar pattern of changes was observed in the number of necrotic hepatocytes. Blood endotoxin and hepatic levels of CD14 messenger RNA (mRNA) and protein were increased by ethanol. This effect was blocked in ovariectomized rats and elevated by estrogen replacement. Moreover, Kupffer cells isolated from ethanol-treated rats with estrogen replacement produced more tumor necrosis factor , (TNF-,) than those from control and ovariectomized rats. It is concluded, therefore, that the sensitivity of rat liver to alcohol-induced injury is directly related to estrogen, which increases endotoxin in the blood and CD14 expression in the liver, leading to increased TNF-, production. [source]

Influence of advanced injection timing on the performance and emissions of CI engine fueled with ethanol-blended diesel fuel

INTERNATIONAL JOURNAL OF ENERGY RESEARCH, Issue 11 2008
Cenk Sayin
Abstract Ethanol has been considered as an alternative fuel for diesel engines. On the other hand, injection timing is a major parameter that sensitively affects the engine performance and emissions. Therefore, in this study, the influence of advanced injection timing on the engine performance and exhaust emissions of a single cylinder, naturally aspirated, four stroke, direct injection diesel engine has been experimentally investigated when using ethanol-blended diesel fuel from 0 to 15% with an increment of 5%. The original injection timing of the engine is 27° crank angle (CA) before top dead center (BTDC). The tests were conducted at three different injection timings (27, 30 and 33° CA BTDC) for 30 Nm constant load at 1800 rpm. The experimental results showed that brake-specific energy consumption (BSEC), brake-specific fuel consumption (BSFC), NOx and CO2 emissions increased as brake-thermal efficiency (BTE), smoke, CO and HC emissions decreased with increasing amount of ethanol in the fuel mixture. Comparing the results with those of original injection timing, NOx emissions increased and smoke, HC and CO emissions decreased for all test fuels at the advanced injection timings. For BSEC, BSFC and BTE, advanced injection timings gave negative results for all test conditions. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Ethanol synthesis from glycerol by Escherichia coli redox mutants expressing adhE from Leuconostoc mesenteroides

JOURNAL OF APPLIED MICROBIOLOGY, Issue 2 2010
P.I. Nikel
Abstract Aims:, Analysis of the physiology and metabolism of Escherichia coli arcA and creC mutants expressing a bifunctional alcohol-acetaldehyde dehydrogenase from Leuconostoc mesenteroides growing on glycerol under oxygen-restricted conditions. The effect of an ldhA mutation and different growth medium modifications was also assessed. Methods and Results:, Expression of adhE in E. coli CT1061 [arcA creC(Con)] resulted in a 1·4-fold enhancement in ethanol synthesis. Significant amounts of lactate were produced during micro-oxic cultures and strain CT1061LE, in which fermentative lactate dehydrogenase was deleted, produced up to 6·5 ± 0·3 g l,1 ethanol in 48 h. Escherichia coli CT1061LE derivatives resistant to >25 g l,1 ethanol were obtained by metabolic evolution. Pyruvate and acetaldehyde addition significantly increased both biomass and ethanol concentrations, probably by overcoming acetyl-coenzyme A (CoA) shortage. Yeast extract also promoted growth and ethanol synthesis, and this positive effect was mainly attributable to its vitamin content. Two-stage bioreactor cultures were conducted in a minimal medium containing 100 ,g l,1 calcium d -pantothenate to evaluate oxic acetyl-CoA synthesis followed by a switch into fermentative conditions. Ethanol reached 15·4 ± 0·9 g l,1 with a volumetric productivity of 0·34 ± 0·02 g l,1 h,1. Conclusions:,Escherichia coli responded to adhE over-expression by funnelling carbon and reducing equivalents into a highly reduced metabolite, ethanol. Acetyl-CoA played a key role in micro-oxic ethanol synthesis and growth. Significance and Impact of the Study:, Insight into the micro-oxic metabolism of E. coli growing on glycerol is essential for the development of efficient industrial processes for reduced biochemicals production from this substrate, with special relevance to biofuels synthesis. [source]

Survival of spores of Rhizopus stolonifer, Aspergillus niger, Botrytis cinerea and Alternaria alternata after exposure to ethanol solutions at various temperatures

JOURNAL OF APPLIED MICROBIOLOGY, Issue 6 2004
F. Mlikota Gabler
Abstract Aims:, To quantify and model the toxicity of brief exposures of spores of Rhizopus stolonifer, Aspergillus niger, Botrytis cinerea and Alternaria alternata to heated, aqueous ethanol solutions. These fungi are common postharvest decay pathogens of fresh grapes and other produce. Sanitation of produce reduces postharvest losses caused by these and other pathogens. Methods and Results:, Spores of the fungi were exposed to solutions containing up to 30% (v/v) ethanol at 25,50°C for 30 s, then their survival was determined by germination on semisolid media. Logistical, second-order surface-response models were prepared for each fungus. Subinhibitory ethanol concentrations at ambient temperatures became inhibitory when heated at temperatures much lower than those that cause thermal destruction of the spores by water alone. At 40°C, the estimated ethanol concentrations that inhibited the germination of 50% (LD50) of the spores of B. cinerea, A. alternata, A. niger and R. stolonifer were 9·7, 13·5, 19·6 and 20·6%, respectively. Conclusions:, Ethanol and heat combinations were synergistic. Control of spores of these fungi could be accomplished with much lower temperatures and ethanol concentrations when combined compared with either used alone. Botrytis cinerea and A. alternata were less resistant to the combination than A. niger or R. stolonifer. [source]

The Dose-Response Effects of Ethanol on the Human Fetal Osteoblastic Cell Line

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2001
A. Maran
Abstract Alcohol is a risk factor for the development of osteoporosis, especially in men. Chronic alcohol abuse decreases bone mass, which contributes to the increased incidence of fractures. To better understand the mechanism of action of ethanol on bone metabolism, we have studied the dose-response effects of ethanol on conditionally immortalized human fetal osteoblasts (hFOB) in culture. Ethanol treatment had no significant effects on osteoblast number after 1 day or 7 days. Ethanol treatment did not reduce type I collagen protein levels at either time point at any dose but slightly reduced alkaline phosphatase activity after 7 days. The messenger RNA (mRNA) levels for alkaline phosphatase, type I collagen, and osteonectin were unaltered by 24 h of ethanol treatment but a high dose (200 mM) reduced mRNA levels for the two bone matrix proteins after 7 days. Ethanol treatment led to dose-dependent increases in transforming growth factor ,1 (TGF-,1) mRNA levels and decreases in TGF-,2 mRNA levels. The concentration of ethanol in the medium decreased with time because of evaporation but there was little degradation caused by metabolism. These results, which show that cultured osteoblasts are less sensitive than osteoblasts in vivo, suggest that the pronounced inhibitory effects of ethanol on bone formation are not caused by direct cell toxicity. [source]

p38SJ, a novel DINGG protein protects neuronal cells from alcohol induced injury and death

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2009
Shohreh Amini
Ethanol induces neuronal cell injury and death by dysregulating several signaling events that are controlled, in part, by activation of MAPK/ERK1/2 and/or inactivation of its corresponding phosphatase, PP1. Recently, we have purified a novel protein of 38,kDa in size, p38SJ, from a callus culture of Hypericum perforatum, which belongs to an emerging DINGG family of proteins with phosphate binding activity. Here, we show that treatment of neuronal cells with p38SJ protects cells against injury induced by exposure to ethanol. Furthermore, pre-treatment of neuronal cells with p38SJ diminishes the level of the pro-apoptotic protein Bax and some events associated with apoptosis such as caspase 3 cleavage. In addition, by inducing stress, alcohol can elevate production of reactive oxygen species (ROS) that leads to a decrease in the activity of superoxide dismutase (SOD). Our results showed that p38SJ restores the activity of SOD in the ethanol treated neuronal cells. These observations provide a novel biological tool for developing new approaches for preventing neuronal cell death induced by ethanol and possibly treatment of neurological disorders associated with alcohol abuse. J. Cell. Physiol. 221: 499,504, 2009. © 2009 Wiley-Liss, Inc. [source]

Direct and correlated responses to selection for larval ethanol tolerance in Drosophila melanogaster

JOURNAL OF EVOLUTIONARY BIOLOGY, Issue 2 2001
J. D. Fry
Ethanol is an important larval resource and toxin for natural Drosophila melanogaster populations, and ethanol tolerance is genetically variable within and among populations. If ethanol-tolerant genotypes have relatively low fitness in the absence of ethanol, as suggested by the results of an earlier study, genetic variation for ethanol tolerance could be maintained by variation in ethanol levels among breeding sites. I selected for ethanol tolerance in large laboratory populations by maintaining flies on ethanol-supplemented media. After 90 generations, the populations were compared with control populations in egg-to-adult survival and development rate on ethanol-supplemented and unsupplemented food. When compared on ethanol-supplemented food, the ethanol-selected populations had higher survival and faster development than the control populations, but on unsupplemented food, the populations did not differ in either trait. These results give no evidence for a ,trade-off' between the ability to survive and develop rapidly in the presence of ethanol and the ability to do so in its absence. The effect of physiological induction of ethanol tolerance by exposing eggs to ethanol was also investigated; exposing eggs to ethanol strongly increased subsequent larval survival on ethanol-supplemented food, but did not affect survival on regular food, and slowed development on both ethanol-supplemented and regular food, partly by delaying egg hatch. [source]

The effects of preservation on fish tissue stable isotope signatures

JOURNAL OF FISH BIOLOGY, Issue 6 2006
B. Kelly
The effects of formalin and ethanol preservation on the ,13C and ,15N isotope signatures of Arctic charr Salvelinus alpinus muscle tissue were examined. The lipid content of the tissue samples studied ranged from 3·6 to 6·1% and was not correlated with the magnitude of observed isotopic shifts in preserved samples. Ethanol and formalin significantly depleted and enriched, respectively, the ,13C isotope signatures of preserved tissues when compared to control samples. Ethanol did not significantly enrich ,15N signatures in comparison to controls, whereas formalin did. A meta-analysis of multiple species effects further demonstrated significant preservation effects in fish tissue. Statistical analysis of data obtained by correcting preserved tissue isotope signatures with literature, bootstrapped or meta-analysis derived correction factors demonstrated significant differences between corrected and control sample isotope signatures or failure to produce a unity slope when the data sets were regressed against one another. Species-specific, bootstrapped linear correction models resulted in no such errors. Results suggest that species-specific correction methods should be used for fishes because of the known wide variation in fish tissue lipid content and composition. Accordingly, the use of pilot studies will be required to develop correction factors that properly adjust for preservation effects when interpreting temporal patterns in historic analyses of food webs. [source]

ANALYSIS OF VARIABLES AND MODELING OF GEVUINA AVELLANA OIL EXTRACTION WITH ETHANOL NEAR AZEOTROPE CONDITIONS

Purification and Characterization of an ,-L-Rhamnosidase from Aspergillus terreus of Interest in Winemaking

JOURNAL OF FOOD SCIENCE, Issue 2 2001
M.V. Gallego
ABSTRACT: An enzyme with ,-L-rhamnosidase activity was purified to homogeneity from a culture filtrate of Aspergillus terreus after growth in a medium containing L-rhamnose as the sole carbon source. The biosynthesis of this enzyme was repressed by glucose. The enzyme had a molecular mass of 96 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis and an isoelectric point of 4.6 as determined by analytical isoelectric focusing. The pH and temperature optima for the enzyme were found to be 4.0 and 44 °C, respectively. Using p-nitrophenyl-,-L-rhamnopyranoside as a substrate, the enzyme exhibited Michaelis-Menten kinetics with KM and Vmax values of 0.17 mM and 84 U/mg, respectively. The enzyme was inhibited competitively by L-rhamnose (K1 2.5 mM). Divalent cations such as Ca2+ Mg2+ Zn2+ and Co2+ stimulated the a-L-rhamnosidase activity, whereas this was inhibited by Hg2+ and Cd2+. Ethanol (12% v/v) and glucose (21% w/v) decreased enzyme activity by approximately 20%, while this was not affected by SO2. [source]

Ethanol inhibits cold-menthol receptor TRPM8 by modulating its interaction with membrane phosphatidylinositol 4,5-bisphosphate

JOURNAL OF NEUROCHEMISTRY, Issue 1 2007
Jan Benedikt
Abstract Ethanol has opposite effects on two members of the transient receptor potential (TRP) family of ion channels: it inhibits the cold-menthol receptor TRPM8, whereas it potentiates the activity of the heat- and capsaicin-gated vanilloid receptor TRPV1. Both thermosensitive cation channels are critically regulated by the membrane lipid, phosphatidylinositol 4,5-bisphosphate (PIP2). The effects of this phospholipid on TRPM8 and TRPV1 are also functionally opposite: PIP2 is necessary for the activation of TRPM8 but it constitutively inhibits TRPV1. This parallel led us to investigate the possible role of PIP2 in the ethanol-induced modulation of rat TRPM8, heterologously expressed in HEK293T cells. In this study, we characterize the effects of ethanol (0.1,10%) on whole-cell currents produced by menthol and by low temperature (< 17°C). We show that the inclusion of PIP2 in the intracellular solution results in a strong reduction in the ethanol-induced inhibition of menthol-evoked responses. Conversely, intracellular dialysis with anti-PIP2 antibody or with the PIP2 scavenger, poly l -lysine, enhanced the ethanol-induced inhibition of TRPM8. A 20 min pre-incubation with wortmannin caused a modest decrease in inhibition produced by 1% ethanol, indicating that the ethanol-induced inhibition is not mediated by lipid kinases. These findings suggest that ethanol inhibits TRPM8 by weakening the PIP2,TRPM8 channel interaction; a similar mechanism may contribute to the ethanol-mediated modulation of some other PIP2 -sensitive TRP channels. [source]

Ethanol enhancement of cocaine- and amphetamine-regulated transcript mRNA and peptide expression in the nucleus accumbens

JOURNAL OF NEUROCHEMISTRY, Issue 2 2006
Armando Salinas
Abstract Cocaine- and amphetamine-regulated transcript (CART) is a peptide neurotransmitter that has been implicated in drug reward and reinforcement. CART mRNA and peptide expression are highly concentrated in several compartments of the mesolimbic reward pathway. Several lines of evidence suggest that CART peptides may contribute to rewarding behaviors and the addiction liability of psychostimulants; however, there are no reports of basic work concerning CART in relation to alcohol and mechanisms of alcohol dependence development. Therefore, in this study we investigated the response of CART transcript and peptide to acute ethanol administration in vivo. Rats were administered ethanol (1 g/kg or 3.5 g/kg, 1 h, ip) and CART expression was measured by RT-PCR in the nucleus accumbens (NAcc). Ethanol (3.5 g/kg) increased CART transcription markedly. The interactions of dopamine on ethanol-induced CART expression were further evaluated pharmacologically using D1 and D2/D3 receptor antagonists. Both SCH 23390 (0.25 mg/kg) or raclopride (0.2 mg/kg) pre-treatment significantly suppressed ethanol-enhancement of CART mRNA transcription. Confocal immunofluorescence microscopy revealed that CART peptide immunoreactivity was also enhanced in both the core and the shell of the NAcc by ethanol administration. These findings demonstrate that CART mRNA and peptide expression are responsive to acute ethanol administrated in vivo and suggests that CART peptides may be important in regulating the rewarding and reinforcing properties of ethanol. [source]

Ethanol potentiates the function of the human dopamine transporter expressed in Xenopus oocytes

JOURNAL OF NEUROCHEMISTRY, Issue 5 2001
R. Dayne Mayfield
Ethanol alters a variety of properties of brain dopaminergic neurons including firing rate, synthesis, release, and metabolism. Recent studies suggest that ethanol's action on central dopamine systems may also involve modulation of dopamine transporter (DAT) activity. The human DAT was expressed in Xenopus oocytes to examine directly the effects of ethanol on transporter function. [3H]Dopamine (100 nm) accumulation into DAT-expressing oocytes increased significantly in response to ethanol (10 min; 10,100 mm). In two-electrode voltage-clamp experiments, DAT-mediated currents were also enhanced significantly by ethanol (10,100 mm). The magnitude of the ethanol-induced potentiation of DAT function depended on ethanol exposure time and substrate concentration. Cell surface DAT binding ([3H]WIN 35,428; 4 nm) also increased as a function of ethanol exposure time. Thus, the increase in dopamine uptake was associated with a parallel increase in the number of DAT molecules expressed at the cell surface. These experiments demonstrate that DAT-mediated substrate translocation and substrate-associated ionic conductances are sensitive to intoxicating concentrations of ethanol and suggest that DAT may represent an important site of action for ethanol's effects on central dopaminergic transmission. A potential mechanism by which ethanol acts to enhance DAT function may involve regulation of DAT expression on the cell surface. [source]

The Interaction of Gestational and Postnatal Ethanol Experience on the Adolescent and Adult Odor-Mediated Responses to Ethanol in Observer and Demonstrator Rats

ALCOHOLISM, Issue 10 2010
Amber M. Eade
Background:, Gestational ethanol exposure enhances the adolescent reflexive sniffing response to ethanol odor. Postnatal exposures of naïve animals as either an observer (i.e., conspecific) or demonstrator (i.e., intoxicated peer) using a social transmission of food odor preference paradigm also yields enhanced odor-mediated responses. Studies on the interaction of fetal and postnatal exposures using the social transmission paradigm have been limited to the responses of observers. When combined, the enhanced response is greater than either form of exposure alone and, in observer females, yields adult persistence. The absence of a male effect is noteworthy, given that chemosensory mechanisms are suggested to be an important antecedent factor in the progression of ethanol preference. Observers gain odor information on the breath of the demonstrator through social interaction. Demonstrators experience the pharmacologic properties of ethanol along with retronasal and hematogenic olfaction. Thus, we tested whether augmentation of the fetal ethanol-induced behavioral response with postnatal exposure as a demonstrator differed from that as an observer. We also examined whether re-exposure as a demonstrator yields persistence in both sexes. Methods:, Pregnant dams were fed an ethanol containing or control liquid diet throughout gestation. Progeny received four ethanol or water exposures: one every 48 hours through either intragastric infusion or social interaction with the infused peer beginning on P29. The reflexive behavioral sniffing response to ethanol odor was tested at postnatal (P) day 37 or P90, using whole-body plethysmography. Results:, When tested in either adolescence or adulthood - fetal ethanol exposed adolescent ethanol observers and demonstrators significantly differed in their odor-mediated response to ethanol odor both between themselves and from their respective water controls. Nonetheless, adolescent ethanol re-exposure as a demonstrator, like an observer, enhanced the reflexive sniffing response to ethanol odor at both testing ages by augmenting the known effects of prior fetal ethanol experience. At each age, the magnitude of the enhanced odor response in demonstrators was similar to that of observers. Interestingly, only re-exposure as a demonstrator resulted in persistence of the behavioral response into adulthood in both sexes. Conclusions:, The method of ethanol re-exposure plays an important role in prolonging the odor-mediated effects of fetal exposure. While ethanol odor-specific exposure through social interaction is important, additional factors such as the pairing of retronasal and hematogenic olfaction with ethanol's intoxicating properties appear necessary to achieve persistence in both sexes. [source]

Ethanol Alters the Osteogenic Differentiation of Amniotic Fluid-Derived Stem Cells

ALCOHOLISM, Issue 10 2010
Jennifer A. Hipp
Background:, Fetal alcohol spectrum disorder (FASD) is a set of developmental defects caused by prenatal alcohol exposure. Clinical manifestations of FASD are highly variable and include mental retardation and developmental defects of the heart, kidney, muscle, skeleton, and craniofacial structures. Specific effects of ethanol on fetal cells include induction of apoptosis as well as inhibition of proliferation, differentiation, and migration. This complex set of responses suggests that a bioinformatics approach could clarify some of the pathways involved in these responses. Methods:, In this study, the responses of fetal stem cells derived from the amniotic fluid (AFSCs) to treatment with ethanol have been examined. Large-scale transcriptome analysis of ethanol-treated AFSCs indicates that genes involved in skeletal development and ossification are up-regulated in these cells. Therefore, the effect of ethanol on osteogenic differentiation of AFSCs was studied. Results:, Exposure to ethanol during the first 48 hours of an osteogenic differentiation protocol increased in vitro calcium deposition by AFSCs and increased alkaline phosphatase activity. In contrast, ethanol treatment later in the differentiation protocol (day 8) had no significant effect on the activity of alkaline phosphatase. Conclusions:, These results suggest that transient exposure of AFSCs to ethanol during early differentiation enhances osteogenic differentiation of the cells. [source]