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PubMed1977

Comparison of ethanol, pentobarbital, and phenobarbital using drug vs. drug discrimination training.

Rats learned drug vs. drug (D vs. D) or drug vs. no drug (D vs. N) discriminations in a T-maze shock escape task with various doses of pentobarbital, phenobarbital, or ethanol. Dose-effect curves were obtained for each drug using D vs. N training. After D vs. N training with any one of these drugs, rats made D choices during substitution tests with the other two drugs, suggesting drug interchangeability. D vs. D training also showed that pentobarbital and phenobarbital were virtually indistinguishable from one another. However, ethanol was readily discriminated from pentobarbital, showing that the two drugs differed. The results show the utility of D vs. D training as a method for studying drug differences that may be too small to detect with substitution tests.

Animals↗

PubMedDate not supplied

[Beta-galactosidase activity of strains of Kluyveromyces spp. and production of ethanol from lactose].

We investigated the behavior of yeast of the genus Kluyveromyces (K. fragilis 507, K. lactis 29 and K. lactis 10), which grow on lactose as sole carbon source, since they possess an enzyme system for the utilization of this sugar. We determined the beta-galactosidase activity of these strains, grown in the logarithmic phase in media containing glucose and lactose. On addition of 0 to 12% v/v ethanol to cells treated with toluene, we did not observe inhibition of the enzyme in strain 10 of Kluyveromyces lactis, which showed the greatest activity (704.4 Units). Since there exist the possibility of industrial utilization of concentrated whey (4 times), we performed fermentation tests of the three strains, at 30 C, in media containing initial lactose concentrations of 16.5 and 24.5%. After 48 h the residual lactose concentration was practically zero, and the ethanol concentrations had reached 7.60 and 10.10% v/v. It might be expected that the rate of fermentation of a disaccharide such as lactose would be related to the rate of hydrolysis of the sugar, so that strains having a higher rate of enzymatic hydrolysis should show a higher fermentation rate. However, we did not observe such behavior, as strains of Kluyveromyces having enzymatic activities as different as K. lactis 10 (704.4 U) and K. lactis 29 (189.7 U) did not show any great difference in the production of ethanol from lactose.

Ethanol↗

PubMed1991

Perspectives: do alcohol calories count?

Chronic consumption of substantial amounts of alcohol is not associated with the expected effect on body weight. Isocaloric substitution of carbohydrates by ethanol results in weight loss, and addition of ethanol to an otherwise normal diet does not produce the expected weight gain. This energy deficit cannot be explained by maldigestion or malabsorption but has been attributed to induction of the microsomal ethanol oxidizing system (a metabolic pathway that oxidizes ethanol without associated chemical energy production), increased sympathetic tone and associated thermogenesis, and/or enhanced ATP breakdown (with increased purine catabolism) secondary to the acetate produced from ethanol. All these hypotheses do not fully explain the lack of weight deficit when alcohol is consumed with a very-low-fat diet, which suggests that an alteration in the energy utilization derived from fat plays a major role, possibly through uncoupling of oxidation with phosphorylation in mitochondria damaged by chronic ethanol consumption.

Adult↗

PubMed1995

ESBRA 1994 Award Lecture. Phosphatidylethanol formation: specific effects of ethanol mediated via phospholipase D.

Phosphatidylethanol is a unique phospholipid which is formed in cell membranes only in the presence of ethanol. The reaction is catalysed by phospholipase D, an enzyme that normally catalyses the hydrolysis of phospholipids leading to the formation of phosphatidic acid. However, phospholipase D also utilizes short-chain alcohols as substrates resulting in the formation of the corresponding phosphatidylalcohol. This is a specific mechanism through which ethanol may interact with cell function. Phospholipase D is activated by several different receptors and has during recent years been suggested to play a role in cellular signalling. Secretory processes as well as long-term changes of cell function have been associated with the activation of phospholipase D. Since ethanol competes with water as a substrate for this enzyme, phosphatidylethanol is formed at the expense of the normal lipid product, phosphatidic acid, in an ethanol concentration-dependent manner. Therefore, the phospholipase D-mediated signal transduction diverges from production of the normal signalling lipid in the presence of ethanol. However, phosphatidic acid may also be formed by other pathways and their relative contribution to the formation of this lipid depends on the cell and receptor type. Thus, it is important to identify the signalling systems where phospholipase D dominates the lipid messenger production since these may be especially vulnerable to ethanol. In addition to a change in phospholipase D-mediated signal transduction, accumulation of phosphatidylethanol in cell membranes may also induce disturbances in cell function. Significant amounts of this abnormal phospholipid have been detected after ethanol exposure in brain and other organs from rat, in cultured cells as well as in human blood cells. The degradation of phosphatidylethanol is relatively slow and it remains in the cells after ethanol has disappeared. It is possible that an abnormal phospholipid that accumulates in cell membranes affects membrane-associated processes. Phosphatidylethanol is a lipid with a small, anionic head group and its biophysical properties are different compared with other phospholipids. Moreover, this lipid has been demonstrated to influence membrane characteristics, enzyme activities and levels of signalling molecules. Thus, both the inhibition of phospholipase D-mediated signal transduction and the accumulation of phosphatidylethanol represent possible pathways through which ethanol may disturb cell function.

Animals↗

PubMed1977

Incorporation of the 1-pro-R and the 1-pro-S hydrogen atoms of ethanol into steroids and phosphatidylcholines in vivo.

The transfer of deuterium from chiral 1-monodeuteroethanols to various metabolites formed in the liver was studied in order to investigate the coupling of metabolic reductions to the alcohol dehydrogenase and the aldehyde dehydrogenase reactions. The ethanols were administered to female bile fistula rats for 10 h. The hydrogen at C-2 in the glycerol moiety of newly formed phosphatidylcholine molecules in bile, liver and plasma was derived to 22-25% from the 1-pro-R position and to 5-6% from the 1-pro-S position in the ethanol. sn-Glycerol 3-phosphate isolated from liver had a lower deuterium content at C-2. The ratio between the contributions from the two positions in ethanol to C-2 of free sn-glycerol 3-phosphate was the same as in the phosphatidylcholines. This indicates that the higher degree of labelling of this position in phosphatidylcholines is not due to a specific coupling between alcohol dehydrogenase and the formation of a phosphatidylcholine precursor. Cholesterol and chenodeoxycholic acid in bile became increasingly labelled, and the ratio between the incorporations from the 1-pro-S and the 1-pro-R positions of ethanol was about 0.37 in cholesterol and 0.46 in chenodeoxycholic acid. Thus, these NADPH-dependent reactions utilized hydrogen from the 1-pro-S position to a larger extent than NADH-dependent reactions.

Animals↗

PubMed2000

The role of metabolic engineering in the improvement of Saccharomyces cerevisiae: utilization of industrial media.

Metabolic engineering has become a very important approach to strain improvement in parallel with classical strain development. Although Saccharomyces cerevisiae has been domesticated for ethanol and bread production, there are still some fundamental problems associated with its industrial use. The industrially used carbon sources often consist of a sugar mixture, and due to glucose repression these sugars are utilized sequentially, resulting in prolonged production time. In this article we discuss the application of metabolic engineering for construction of glucose-derepressed strains and specify advantages as well as difficulties associated with this approach.

Journal Article↗

PubMed2003

Fatty acid ethyl esters. Ethanol metabolites that reflect ethanol intake.

Fatty acid ethyl esters (FAEEs) are nonoxidative ethanol metabolites that have been implicated as mediators of alcohol-induced organ damage. FAEEs are detectable in the blood after ethanol ingestion, and on that basis represent markers of ethanol intake. FAEEs have also been quantitated in human liver and adipose tissue and have been shown to be postmortem markers of premortem ethanol intake. A substantial difference in FAEE concentration was found in liver and adipose tissue of patients with detectable blood ethanol at the time of autopsy vs those with no detectable blood ethanol, who were either chronic alcoholics or social drinkers. Most currently available diagnostic markers for chronic alcoholism have limited clinical utility. Data in this report demonstrate that the amount or type of FAEEs can be used to differentiate a chronic alcoholic from an episodic heavy drinker (binage drinker) at or near peak blood ethanol concentrations and approximately 24 hours after discontinuation of ethanol. Thus, FAEEs are markers of ethanol intake in blood and tissues and can be useful in distinguishing chronic alcoholics from binge drinkers.

Alcoholic Intoxication↗

PubMed2002

From yeast genetics to biotechnology.

Roots of classical yeast genetics go back to the early work of Lindegreen in the 1930s, who studied thallism, sporulation and inheritance of wine yeast strains belonging to S. cerevisiae. Consequent mutation and hybridization of heterothallic S. cerevisae strains resulted in the discovery of life cycle and mating type system, as well as construction of the genetic map. Elaboration of induced mutation and controlled hybridization of yeast strains opened up new possibilities for the genetic analysis of technologically important properties and for the production of improved industrial strains, but a big drawback was the widely different genetic properties of laboratory and industrial yeast strains. Genetic analysis and mapping of industrial strains were generally hindered because of homothallism, poor sporulation and/or low spore viability of brewing and wine yeast strains [1, 2]. In spite of this, there are a few examples of the application of sexual hybridization in the study of genetic control of important technological properties, e.g. sugar utilization, flocculation and flavor production in brewing yeast strains [3] or in the improvement of ethanol producing S. cerevisiae strains [4]. Rare mating and application of karyogamy deficient (kar-) mutants also proved useful in strain improvement [5]. Importance of yeasts in biotechnology is enormous. This includes food and beverage fermentation processes where a wide range of yeast species are playing role, but S. cerevisiae is undoubtedly the most important species among them. New biotechnology is aiming to improve these technologies, but besides this, a completely new area of yeast utilization has been emerged, especially in the pharmaceutical and medical areas. Without decreasing the importance of S. cerevisiae, numerous other yeast species, e.g. Kluyveromyces lactis, Hansenula polymorpha, Pichia pastoris, Schizosaccharomyces pombe and Yarrowia lipolytica have gained increasing potentialities in the modern fermentation biotechnology [6]. Developments in yeast genetics, biochemistry, physiology and process engineering provided bases of rapid development in modern biotechnology, but elaboration of the recombinant DNA technique is far the most important milestone in this field. Other molecular genetic techniques, as molecular genotyping of yeast strains proved also very beneficial in yeast fermentation technologies, because dynamics of both the natural and inoculated yeast biota could be followed by these versatile DNA-based techniques.

Biotechnology↗

PubMed2000

Continuous fermentation studies with xylos-utilizing recombinant Zymomonas mobilis.

This study examined the continuous cofermentation performance characteristics of a dilute-acid "prehydrolysate-adapted" recombinant Zymomonas 39676:pZB4L and builds on the pH-stat batch fermentations with this recombinant that we reported on last year. Substitution of yeast extract by 1% (w/v) corn steep liquor (CSL) (50% solids) and Mg (2 mM) did not alter the cofermentation performance. Using declared assumptions, the cost of using CSL and Mg was estimated to be 12.5 cents/gal of ethanol with a possibility of 50% cost reduction using fourfold less CSL with 0.1% diammonium phosphate. Because of competition for a common sugar transporter that exhibits a higher affinity for glucose, utilization of glucose was complete whereas xylose was always present in the chemostat effluent. The ethanol yield, based on sugar used, was 94% of theoretical maximum. Altering the sugar ratio of the synthetic dilute acid hardwood prehydrolysate did not appear to significantly change the pattern of xylose utilization. Using a criterion of 80% sugar utilization for determining the maximum dilution rate (Dmax), changing the composition of the feed from 4% xylose to 3%, and simultaneously increasing the glucose from 0.8 to 1.8% shifted Dmax from 0.07 to 0.08/h. With equal amounts of both sugars (2.5%), Dmax was 0.07/h. By comparison to a similar investigation with rec Zm CP4:pZB5 with a 4% equal mixture of xylose and glucose, we observed that at pH 5.0, the Dmax was 0.064/h and shifted to 0.084/h at pH 5.75. At a level of 0.4% (w/v) acetic acid in the CSL-based medium with 3% xylose and 1.8% glucose at pH 5.75, the Dmax for the adapted recombinant shifted from 0.08 to 0.048/h, and the corresponding maximum volumetric ethanol productivity decreased 45%, from 1.52 to 0.84 g/(L.h). Under these conditions of continuous culture, linear regression of a Pirt plot of the specific rate of sugar utilization vs D showed that 4 g/L of acetic acid did not affect the maximum growth yield (0.030 g dry cell mass/g sugar), but did increase the maintenance coefficient twofold, from 0.46 to 1.0 g of sugar/(g of cell.h).

Biotechnology↗

PubMed1979

Sources of energy for the brain and physical dependence on ethanol.

This paper describes a proposed biochemical mechanism to account for physical dependence on ethanol. Long-term exposure to a continuous and plentiful supply of ethanol-derived hydrogens in NADH and ethanol-derived acetyl-CoA (AcCoA) may lead to a decreased rate of production of endogenous hydrogens in NADH and endogenous AcCoA in compensation. It is proposed that physical dependence on ethanol occurs when ketolytic- and glycolytic-based NADH and AcCoA synthetic rates fall below the rate of utilization by the brain; the brain then "depends" on alcohol-derived NADH and AcCoA for normal function.

Acetyl Coenzyme A↗

PubMed1989

Evidential breath ethanol analyzers, accuracy and sensitivity to breath acetone.

The purposes of this study included the examination of the relative accuracy of a number of evidential breath analyzers available in the United States, the sensitivity of ethanol breath analyzers to simulated breath acetone and the generation and subsequent interference created by endogenous acetone. This study used both laboratory simulation and human ethanol testing as well as a systematic examination of the sensitivity of various ethanol breath test instruments to both endogenous and simulated breath acetone. The results suggest that when evidential breath ethanol testers are administered in a uniform fashion, consistent and reliable results occur. Further, endogenous and simulated breath acetone can effect infrared ethanol breath testers but at levels in the case of endogenous acetone, in a non-significant fashion. Simulated breath acetone, consistent with other research produced selective interference on evaluation of breath instruments. The instruments utilizing wavelength 3.4 microns infrared bands were affected the greatest. Endogenous breath and blood acetone was demonstrated in a non-diabetic. The resulting breath acetone levels did produce mimicked ethanol levels on all single wavelength (3.4 microns range) instruments. Nine micron IR range instruments and the Breathalyzer 900 which utilizes a wet chemical procedure were unaffected by endogenous acetone. Those instruments equipped with acetone detectors, found in certain instruments, did not identify endogenously produced acetone.

Accidents, Traffic↗

PubMed2005

Disruption of cholesterol homeostasis in the developing brain as a potential mechanism contributing to the developmental neurotoxicity of ethanol: an hypothesis.

While excess cholesterol may have deleterious consequences, as in the case of atherosclerosis, too little cholesterol may endanger the development of the brain. Different degrees of mental retardation are often observed in inborn errors of cholesterol synthesis, such as the Smith-Lemli-Opitz syndrome or in maternal phenylketonuria, where the metabolite of accumulating phenylalanine, phenylacetate, is an inhibitor of cholesterol synthesis. Lack of cholesterol during brain development as a consequence of these genetic defects leads to severe brain damage, microencephaly and mental retardation, which are also hallmarks of the fetal alcohol syndrome (FAS). The brain relies on the in situ synthesis of cholesterol, which occurs mostly in astrocytes. Astrocyte-produced cholesterol is utilized for cell proliferation, or is released, via astrocyte-secreted high density lipoprotein-like particles containing apolipoprotein E, outside the cell, where it is taken up and utilized by neurons for dendrite outgrowth and to form synapses. We propose the hypothesis that ethanol may disrupt cholesterol homeostasis during brain development, and that this effect may be responsible, at least in part, for the central nervous system dysfunctions observed in the FAS, which include altered astrocyte proliferation, neuronal death and diminished synaptic contacts.

Alcohol-Induced Disorders, Nervous System↗

PubMed1980

Antagonism of ethanol's central stimulation by catecholamine receptor agonists.

The effect of ethanol (2 g/kg) on brain catecholamine neurons in the rat as well as its interaction with catecholamine receptor agonists was studied utilizing single unit recording techniques. Identified dopamine (DA) neurons of the zona compacta, substantia nigra as well as noradrenaline (NA) neurons of the locus coeruleus showed no alterations in firing rate at ethanol administration. Also the function of their presynaptic DA and NA receptors, respectively, appeared normal judging from the unaltered inhibitory response to systemically or microiontophoretically applied receptor agonists, apomorphine and clonidine, respectively, when applied in small doses. In contrast, the catecholamine releasing agent amphetamine caused inhibition of firing of the central catecholamine neurons in the same anesthetized preparation. The rate of tryosine hydroxylation in vivo in central DA and NA neurons measured as the amount of Dopa accumulated in various brain regions following inhibition of aromatic l-amino acid decarboxylase by NSD 1015, 150 md/kg i.p., was significantly increased by ethanol in anesthetized rats. Consequently, the present data do not support the hypothesis derived largely from behavioural evidence that ethanol causes inactivation of central DA and NA neurons. The antagonism by catecholamine receptor agonists, apomorphine and clonidine of ethanol's behaviourally stimulant action may thus be of unspecific character. The results indicate that alterations in tyrosine hydroxylase activity, when measured as Dopa formation after decarboxylase inhibition, can occur without concomitantly altered impulse activity in central DA or NA neurons. At present the action of ethanol on brain DA and NA neurons remains unclear and necessitates further studies.

Animals↗

PubMed1999

Photoproduction of hydrogen from raw starch using a halophilic bacterial community.

The bacterial community designated BC1, which originates from night soil treatment sludge, exhibited a strong ability to produce H2 from raw starch in the light in the presence of 3% NaC1. Three halophilic or halotolerant bacterial species, Vibrio fluvialis, Rhodobium marinum, and Proteus vulgaris, were isolated from BC1 and identified. The level of H2 production from starch by coculture of V. fluvialis and R. marinum was nearly equal to that by BC1, indicating that these two strains play roles in starch degradation and H2 production from the degraded products in BC1, respectively. Acetic acid and ethanol, which were detected as the major products of degradation of starch by V. fluvialis in pure culture, seemed to be mainly utilized for H2 production by R. marinum in BC1 and the coculture. However, R. marinum in pure culture could not produce H2 from a synthetic medium containing acetic acid and ethanol, suggesting that V. fluvialis supplied not only substrates but also some unknown factors capable of inducing H2 production from these substrates by R. marinum. A study using the starch-rich microalgae, Chlamydomonas reinhardtii and Dunaliella tertiolecta, demonstrated that the above coculture could be applied to the production of H2 at high yield from raw starch in an algal biomass.

Journal Article↗

PubMed1999

Morphometric and biochemical characteristics of short-term effects of ethanol on rat cardiac muscle.

Alcoholism is a very important cause of congestive cardiomyopathy in man. The aim of this study was to examine a short-term effect of ethanol in rat cardiac muscle, using histologic, morphometric and biochemical methods. Experiments were carried out in Wistar male albino rats, divided into two groups: the control group consisting of eight animals receiving tap water, and the experimental group comprising eight animals received ethyl alcohol for ten days, in a single daily dose of 3 g ethanol/kg body weight, per os, using esophageal intubation. The mean volume weighted nuclear volume of cardiac myocytes was estimated by point sampled intercept method, by objective x 100. The mean cubed nuclear intercept length was multiplied by pi and divided by 3. For biochemical analysis, a 10% water tissue homogenate from the left ventricle was made. In the experimental group, the mean volume-weighted nuclear volume (15.08 +/- 5.20 microm3) was significantly lower than in the control group (51.32 +/- 7.83 microm3) (p < 0.001). The treatment of experimental animals with ethanol caused significant increase of aldolase (p < 0.0001) and aspartate transaminase (p < 0.05) activity in the rat cardiac tissue; at the same time, the enzyme activity of creatine phosphokinase, alanine transaminase and alkaline phosphatase were not changed in the experimental group compared to the control values. The amount of the glucose in the cardiac muscle was greater in the experimental group compared to the control animals. Our results suggest that there is depression of cardiomyocyte nuclei in experimental animals treated with ethanol. Alcohol intake results in the loss of Krebs cycle enzymes and as a consequence there is greater utilization of fatty acids for energy production.

Alcoholism↗

PubMed1993

Effects of chronic ethanol administration on the serotonin-producing cells in rat gastric antral and duodenal mucosa.

The present study describes our observations on optical and ultrastructural features of serotonin-containing cells in the rat antral and upper duodenal mucosa, utilizing optic morphometric measurements in a model of experimental chronic alcoholism of rat in which nutrition was well controlled. Male Wistar rats were given ethanol to provide 23 per cent of the total calories, while starch replaced ethanol isocalorically in controls. Twenty-five per cent of the calories were provided by protein in both groups. Blood levels of serotonin were significantly raised after chronic ethanol feeding (0.059 +/- 0.06 vs. 0.159 +/- 0.012 micrograms/ml, p < 0.01). Decrease in the number of immunohistochemically-detectable serotonin-containing cells was found in the pyloric gland mucosal area specimens of the chronically ethanol-treated rats (68.9 +/- 5.2 vs 43.3 +/- 3.0; p < 0.001). The immunohistologically-evaluated number of the same cells in the duodenal mucosa specimens was significantly decreased by alcohol feeding. Although total villi and crypt count per whole circular section, and the number of crypts per villus were not significantly changed either in control animals or in chronically ethanol-fed rats, decreased number of these cells per whole circular section (289 +/- 21.6 vs. 183 +/- 10.5; p < 0.001) per villus (2.52 +/- 0.14 vs. 1.21 +/- 0.10; p < 0.001) and per crypts (0.97 +/- 0.08 vs. 0.79 +/- 0.04; p < 0.05) were reported after alcohol consumption. In both control and experimental rats the cells were predominantly found in the basal half of the antropyloric mucosa. Alcohol did not lead to any changes in normal distribution of the duodenal serotonin-producing cells. The above quantitative changes in serotonin-producing cells were not accompanied by changes in their subcellular appearance in stomach and duodenal mucosa of alcohol-treated rat.

Alcoholism↗

PubMed2002

Ethanol alters glutamate but not adenosine uptake in rat astrocytes: evidence for protein kinase C involvement.

Glutamate is the primary excitatory neurotransmitter in brain. By stimulating neuronal activity, glutamate increases cellular energy utilization, enhances ATP hydrolysis and promotes the formation of adenosine. Adenosine has receptor-mediated effects that reduce or oppose the excitatory effects of glutamate. As a possible mechanism for ethanol's ability to inhibit excitatory effects of glutamate and enhance inhibitory effects of adenosine, we tested the hypothesis that ethanol promotes [3H]glutamate uptake and inhibits [3H]adenosine uptake. Using primary cultures of rat astrocytes, we found that acute treatment with ethanol (50 mM, 30 min) inhibited [3H]glutamate uptake and reduced protein kinase C (PKC)-induced stimulation of [3H]glutamate uptake. Prolonged treatment (50 mM, 3 day) with ethanol, however, increased both [3H]glutamate uptake and PKC activity. Contrary to other cell types, neither acute or chronic ethanol exposure affected [3H]adenosine uptake in astrocytes. These data indicate that in rat cortical astrocytes ethanol affects [3H]glutamate uptake but not [3H]adenosine uptake by affecting PKC modulation of transporter activity.

Adenosine↗

PubMed1985

Energy metabolism in audiogenically seizure-prone chicks.

Female chicks carrying the lethal, sex-linked recessive paroxysmal (px) gene are susceptible to spontaneous and audiogenic seizures. Because seizure activity does not begin until 1 to 2 weeks posthatching - coincidental with disappearance of the yolk-sac - it is postulated that a contributing factor to seizure activity may be a developmental failure of the chick's ability to switch from lipid to carbohydrate as a primary energy source. In testing this hypothesis, three experiments were performed: 1) to evaluate cerebral energy reserves - adenosine triphosphate (ATP), phosphocreatine - of px and normal chicks; 2) to determine effects of energy source (ethanol, glucose, insulin, and glucose-insulin combined) on audiogenically-induced seizure activity and electrical seizure threshold; 3) to evaluate energy source utilization as estimated by the respiratory quotient (RQ). Brain ATP and phosphocreatine levels in px chicks were both decreased (P less than .05) as early as 10 days posthatching. Ethanol increased electrical seizure threshold in 50% of px chicks and provided protection from audiogenic stimulation. No consistent effect was found with any of the other substances. The RQ of px chicks were lower (P less than .05) than those of controls by 18 days posthatching.

Acoustic Stimulation↗