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Results for “Ethanol utilization”

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At least 253 records · Page 14Linked to original sources
PubMed1977

[Mutants of Pichia guilliermondii yeasts with multiple sensitivity to antibiotics and antimetabolites. I. The selection and properties of the mutants].

Riboflavin deficient mutant Pichia guilliermondii MS1 which requires approximately 1000-fold lower concentration of exogenous vitamin B2 for growth when compared with a non-adapted riboflavin deficient mutants of this species was isolated by means of of UV-irradiation. The growth of the mutant was strongly inhibited by actinomycin D and L-canavanine. The revertant MS8 and MS14 which synthesized riboflavin were selected from the strain MS1. These revertants posses a multiple sensitivity to actinomycin D, rifamycin, euflavine, mitomycin C, antimycin A, 8-azaadenine, 8-azaguanine, L-canavanine and 7-methyl-8-trifluoromethyl-10-(1'-D-ribityl)isoalloxazine. The ability to utilized glycerol and ethanol as a sole carbon source for growth was impaired in these mutants. The mutants which can utilize glycerol were isolated from the strain MS14. Such mutants were resistant to actonomycin D. Mutation (s) which determines a multiple sensitivity and inability to utilized glycerol was recessive.

Anti-Bacterial Agents↗
PubMed1988

Structural and metabolic alterations in rat cerebral cortex induced by prenatal exposure to ethanol.

The effects of prenatal exposure to ethanol on glucose utilization in specific laminae of mature rat cerebral cortex were examined. Pregnant hooded rats were fed a liquid diet containing 35% ethanol-derived calories (E) or pair-fed an isocaloric liquid control diet (C) on gestational days 7-21. The cytoarchitecture of motor areas 4 and 6/8 and of somatosensory areas 3 and 2 of 105 day old, male pups was examined in Cresyl violet-stained sections. The glucose utilization of these cortical regions was assessed using a 2-deoxyglucose autoradiographic technique. Overall, cortex was significantly thinner (5-10%) in E-treated rats than in C-treated rats, but with few exceptions, the thickness of individual laminae was not significantly affected by prenatal treatment. Despite these small structural differences, the overall glucose utilization in areas 4, rostral 6/8 3, and 2 of E-treated rats was significantly less (21-24%) than in C-treated rats. Layer IV was the most affected by the prenatal ethanol exposure (29%) and layers I and VI were the least affected (14-22%). The metabolism of caudal area 6/8 was not significantly affected by gestational exposure to ethanol. These results indicate that thalamic and callosal connections and corticospinal projection neurons are specifically affected by prenatal exposure to ethanol. Such alterations may underlie the learning deficits and motor dysfunction characteristic of fetal alcohol syndrome.

Animals↗
PubMed1975

Effects of ethanol on brain metabolism.

The influence of acute or chronic ethanol administration on the biochemical processes in brain and cerebral metabolic pathways has been discussed. Ethanol seems to affect cerebral carbohydrate metabolism mainly through increased glycogenolysis, although the possibility of decreased cerebral glucose utilization remains eminent. Ethanol affects the consumption of oxygen by the brain tissue presumably through alterations in the brain cell membranes. Inhibition of Na+-K+-ATP-ase observed during ethanol intoxication is suspected to result in alterations in the membranes of the nerve cells. Isotope studies in addition to total respiratory carbon dioxide production strongly suggest the inhibition of citric acid cycle function during ethanol metabolism. Although synthetic pathways for lipids do not seem to be affected by ethanol, lipid oxidation in the cerebral tissue is significantly inhibited. In addition to above mentioned alterations in the cerebral metabolic processes, ethanol also affects ionic transport processes, adenine nucleotides, and amino acid and protein metabolism. The metabolic consequences of such effects of ethanol have been discussed.

Adenosine Diphosphate↗
PubMed2003

[Study on xylose fermentation by Neurospora crassa].

The influence of oxygen limitation and medium initial pH on xylose fermentation by Neurospora crassa AS 3.1602 was investigated. N. crassa AS 3.1602 has high ability of xylose fermentation producing ethanol and xylitol. Oxygen limitation has big influence on ethanol and xylitol production. The maximum conversion rate of ethanol was 63.2% obtained under semi-aerobic conditions. The maximum conversion rate of xylitol was 31.8% obtained under micro-aerobic conditions. Xylitol accumulation is behind the accumulation of ethanol. The optimal pH is 5.0 for ethanol fermentation, and 4.0 for xylitol fermentation, respectively. Xylose fermentation is greatly inhibited at high pH. The yields of ethanol and xylitol are greatly influenced by the initial concentration of xylose. The addition of glucose inhibits both the xylose utilization and the ethanol and xylitol production.

Culture Media↗
PubMed1991

Ethanol potentiates gamma-aminobutyric acid-mediated inhibition in the inferior colliculus: evidence for local ethanol/gamma-aminobutyric acid interactions.

The effect of ethanol on gamma-aminobutyric acid (GABA)-mediated inhibition of neurons of the inferior collicular cortex (IC) was investigated. Systemic administration of 0.5 g/kg ethanol, but not 0.25 g/kg ethanol, potentiated the inhibitory effect of GABA on IC neuronal activity. As with systemic administration of ethanol, local application of two concentrations of ethanol potentiated, in a dose-dependent and concentration-dependent manner, GABA-mediated inhibition of IC activity. When utilizing the lower ethanol concentration (270 mM), increasing ethanol ejection currents produced a correspondingly greater amount of augmentation of GABA inhibition without concomitant changes in spontaneous neural activity. At the highest ejection current tested (90 nA), ethanol doubled the inhibitory effects of GABA on IC neuronal activity. Local application of a higher concentration of ethanol (2.7 M) also potentiated GABA-mediated inhibition, with greater ejection currents producing greater potentiation of GABA-inhibition. Compared to the lower ethanol concentration, the higher ethanol concentration required lower ejection currents to produce comparable amounts of potentiation of GABA inhibition. These findings demonstrate that ethanol potentiates GABA inhibition of IC activity via a local action. In contrast to the effects of ethanol on GABA inhibition, locally applied ethanol failed to potentiate the inhibition by glycine of IC activity, indicating that ethanol does not indiscriminately potentiate all types of inhibition of IC neural activity. Additionally, locally applied ethanol failed to potentiate inhibition by GABA in the lateral septum, indicating that ethanol/GABA interactions are site specific. These findings indicate that ethanol specifically potentiates GABA-mediated inhibition of neural activity, and that this action occurs via a local action at specific sites in brain.

Animals↗
PubMed1980

The effect of chronic ethanol consumption on pathways of ethanol metabolism.

The contribution of the known hepatic pathways for the disposal of ethanol was studied utilizing two different experimental designs. In vitro studies were carried out in hepatocytes isolated from rats fed Purina chow. Rates of ethanol oxidation in these preparations increased with increasing levels of ethanol (10-50 mM). After inhibition of alcohol dehydrogenase (ADH) by pyrazole (2 mM) and the catalase by azide (1 mM) approximately 25% of the ethanol oxidizing activity remained. The residual activity was also dependent upon ethanol concentration and the apparent Km was 13 mM. Hepatocytes from ethanol-fed rats exhibited rates of ethanol oxidation which were also dependent upon the concentration of ethanol. The rates were higher in the hepatocytes from the ethanol-fed rats than in the controls. The addition of inhibitors of ADH and catalase lowered the rates, but abolished neither the differences nor the concentration dependency. In the in vivo studies, ethanol elimination rates were measured in alcohol-fed and control baboons by using a constant ethanol infusion to maintain blood ethanol at three different levels: 5, 10 or 50 mM. Ethanol elimination rate was accelerated with increasing concentration, particularly in alcohol-fed baboons. These observations indicate that a pathway other than the low Km alcohol dehydrogenase participates in alcohol oxidation and is responsible in part for the adaptive increase in ethanol metabolism associated with chronic ethanol consumption.

Alcoholism↗
PubMed2005

Bioreduction of uranium in a contaminated soil column.

The bioreduction of soluble uranium [U(VI)] to sparingly soluble U(IV) species is an attractive remedial technology for contaminated soil and groundwater due to the potential for immobilizing uranium and impeding its migration in subsurface environments. This manuscript describes a column study designed to simulate a three-step strategy proposed for the remediation of a heavily contaminated site at the U.S. Department of Energy's NABIR Field Research Center in Oak Ridge, TN. The soil is contaminated with high concentrations of uranium, aluminum, and nitrate and has a low, highly buffered pH (approximately 3.5). Steps proposed for remediation are (i) flushing to remove nitrate and aluminum, (ii) neutralization to establish pH conditions favorable for biostimulation, and (iii) biostimulation for U(VI) reduction. We simulated this sequence using a packed soil column containing undisturbed aggregates of U(VI)-contaminated saprolite that was flushed with an acidified salt solution (pH 4.0), neutralized with bicarbonate (60 mM), and then biostimulated by adding ethanol. The column was operated anaerobically in a closed-loop recirculation setup. However, during the initial month of biostimulation, ethanol was not utilized, and U(VI) was not reduced. A bacterial culture enriched from the site groundwaterwas subsequently added, and the consumption of ethanol coupled with sulfate reduction immediately ensued. The aqueous concentration of U(VI) initially increased, evidently because of the biological production of carbonate, a ligand known to solubilize uranyl. After approximately 50 days, aqueous U(VI) concentrations rapidly decreased from approximately 17 to <1 mg/L. At the conclusion of the experiment,the presence of reduced solid phase U(IV) was confirmed using X-ray absorption near edge structure spectroscopy. The results indicate that bioreduction to immobilize uranium is potentially feasible at this site; however, the stability of the reduced U(IV) and its potential reoxidation will require further investigation, as do the effects of groundwater chemistry and competitive microbial processes, such as methanogenesis.

Bacteria, Anaerobic↗
PubMed1983

Effects of ethanol on rat hypothalamic luteinizing hormone releasing hormone. A study utilizing radioimmunoassay.

To further understand the mechanism of action by which ethanol (ETOH) decreases plasma luteinizing hormone (LH) levels, the effects of multiple i.p. injections of EOH (1.0--1.5 g/kg) or saline on hypothalamic luteinizing hormone releasing hormone (LHRH) and plasma LH concentrations were evaluated in intact and castrate male rats. After injections, animals were decapitated, brains rapidly removed, and blocks containing the hypothalamus [with median eminence (ME)] were isolated. Hypothalami were subjected to acetic acid extraction and LHRH content quantitated via radioimmunoassay (RIA). Hypothalamic LHRH was found to be inversely correlated with plasma LH. In response to castration, both saline and ETOH-treated rats showed a decrease in hypothalamic LHRH content with a concomitant increase in plasma LH; however, the ETOH-treated animals retained significantly greater concentrations of LHRH and showed significantly lower plasma LH levels when compared to saline-treated controls. Likewise, ETOH-treated intact animals showed significant increases in LHRH content, with LH levels remaining significantly lower than the saline-treated intact controls. Thus, these data from both intact and castrate rats provide evidence to support the hypothesis that alcohol-induced decreases in LH levels are due to a diminished release rate of hypothalamic LHRH.

Animals↗
PubMed2005

Ethanol fermentation from biomass resources: current state and prospects.

In recent years, growing attention has been devoted to the conversion of biomass into fuel ethanol, considered the cleanest liquid fuel alternative to fossil fuels. Significant advances have been made towards the technology of ethanol fermentation. This review provides practical examples and gives a broad overview of the current status of ethanol fermentation including biomass resources, microorganisms, and technology. Also, the promising prospects of ethanol fermentation are especially introduced. The prospects included are fermentation technology converting xylose to ethanol, cellulase enzyme utilized in the hydrolysis of lignocellulosic materials, immobilization of the microorganism in large systems, simultaneous saccharification and fermentation, and sugar conversion into ethanol.

Bacteria↗
PubMed2002

Diverse effects of ethanol on the pathway of inducible prostaglandin E2 production in macrophages.

The effects of ethanol on inducible prostaglandin production in RAW macrophages were investigated. Indomethacin (1 microM) or cycloheximide (1 microM) abolished prostaglandin E2 (PGE2) production induced by lipopolysaccharide (LPS, 1 microg/ml). Ethanol at concentrations from 100 mM to 600 mM concentration-dependently inhibited inducible PGE2 production, while ethanol only at higher concentrations (400 mM or more) showed cytotoxity to the cells. Cyclooxygenase-2 (COX-2) activity, estimated by transformation of exogenous arachidonic acid into PGE2, was not affected by ethanol (100-400 mM). LPS-induced expression of COX-2 mRNA was inhibited by ethanol (50-400 mM). On the other hand, protein expression of COX-2 by LPS was significantly increased by ethanol (100-400 mM). Ethanol alone at concentrations up to 600 mM did not induce expression of COX-2 protein. In a medium containing arachidonic acid (1 microM), ethanol at a low concentration (100 mM) did not significantly affect LPS-induced PGE2 production. These results suggest that ethanol shows diverse effects on the pathway of inducible PGE2 production in macrophages. Finally, ethanol may suppress utilization of arachidonic acid, resulting in reduction of inducible PGE2 production. Further study is needed to elucidate the mechanism of dissociation of ethanol effects on protein and mRNA expression.

Animals↗
PubMed1992

Effects of T-2 toxin on ethanol production by Saccharomyces cerevisiae.

A trichothecene mycotoxin, T-2 toxin, inhibits several aspects of cellular physiology in Saccharomyces cerevisiae, including protein synthesis and mitochondrial functions. We have studied growth of, glucose utilization by, and ethanol production by S. cerevisiae and show that they are inhibited by T-2 toxin between 20 and 200 micrograms/ml in a dose-dependent manner. At 200 micrograms/ml, T-2 toxin causes cell death. This apparent inhibition of ethanol production was found to be the result of growth inhibition. On the basis of biomass or glucose consumption, T-2 toxin increased the amount of ethanol present in the culture. This suggests that T-2 inhibits oxidative but not fermentative energy metabolism by inhibiting mitochondrial function and shifting glucose catabolism toward ethanol formation. As T-2 toxin does not directly inhibit ethanol production by S. cerevisiae, this system could be used for ethanol production from trichothecene-contaminated grain products.

Cell Division↗
PubMed2006

Synaptic GABAergic and glutamatergic mechanisms underlying alcohol sensitivity in mouse hippocampal neurons.

This study was designed to examine the neuronal mechanisms of ethanol sensitivity by utilizing inbred short sleep (ISS) and inbred long sleep (ILS) mouse strains that display large differences in sensitivity to the behavioural effects of ethanol. Comparisons of whole-cell electrophysiological recordings from CA1 pyramidal neurons in hippocampal slices of ISS and ILS mice indicate that ethanol enhances GABAA receptor-mediated inhibitory postsynaptic currents (GABAA IPSCs) and reduces NMDA receptor-mediated excitatory postsynaptic currents (NMDA EPSCs) in a concentration- and strain-dependent manner. In ILS neurons, these receptor systems are significantly more sensitive to ethanol than those in ISS neurons. To further examine the underlying mechanisms of differential ethanol sensitivities in these mice, GABAB activity and presynaptic and postsynaptic actions of ethanol were investigated. Inhibition of GABAB receptor function enhances ethanol-mediated potentiation of distal GABAA IPSCs in ILS but not ISS mice, and this blockade of GABAB receptor function has no effect on the action of ethanol on NMDA EPSCs in either mouse strain. Thus, subregional differences in GABAB activity may contribute to the differential ethanol sensitivity of ISS and ILS mice. Moreover, analysis of the effects of ethanol on paired-pulse stimulation, spontaneous IPSC events, and brief local GABA or glutamate application suggest that postsynaptic rather than presynaptic mechanisms underlie the differential ethanol sensitivity of these mice. Furthermore, these results provide essential information to focus better on appropriate target sites for more effective drug development for the treatment of alcohol abuse.

Animals↗
PubMed1988

Attenuation and cross-attenuation in taste aversion learning in the rat: studies with ionizing radiation, lithium chloride and ethanol.

The preexposure paradigm was utilized to evaluate the similarity of ionizing radiation, lithium chloride and ethanol as unconditioned stimuli for the acquisition of a conditioned taste aversion. Three unpaired preexposures to lithium chloride (3.0 mEq/kg, IP) blocked the acquisition of a taste aversion when a novel sucrose solution was paired with either the injection of the same dose of lithium chloride or exposure to ionizing radiation (100 rad). Similar pretreatment with radiation blocked the acquisition of a radiation-induced aversion, but had no effect on taste aversions produced by lithium chloride (3.0 or 1.5 mEq/kg). Preexposure to ethanol (4 g/kg, PO) disrupted the acquisition of an ethanol-induced taste aversion, but not radiation- or lithium chloride-induced aversions. In contrast, preexposure to either radiation or lithium chloride attenuated an ethanol-induced taste aversion in intact rats, but not in rats with lesions of the area postrema. The results are discussed in terms of relationships between these three unconditioned stimuli and in terms of implications of these results for understanding the nature of the proximal unconditioned stimulus in taste aversion learning.

Animals↗
PubMed1990

The effect of in vitro ethanol exposure on LHRH release from perifused rat hypothalami.

A variety of indirect data suggest that the luteinizing hormone (LH) lowering effects of ethanol (ETOH) are mediated at a hypothalamic level decreasing the synthesis and/or release of LH-releasing hormone (LHRH). Little direct data support this concept, however. The current study was, therefore, designed utilizing a perifusion system with frequent sampling for LHRH with and without ethanol added to determine if ethanol had a direct effect on basal or stimulated LHRH release. A variety of secretagogues, including dopamine, norepinephrine, naloxone, prostaglandin E2, and a high dose of potassium were utilized. Ethanol at a dose of 300 mg% did not alter either basal or secretagogue-stimulated LHRH release from the hypothalami of ethanol-naive male rats. Thus, ethanol did not appear to have a direct effect on LHRH in this system. Alterations in LHRH release by ethanol may occur at a suprahypothalamic level, involving neurotransmitter-LHRH interactions. Alternatively, the well-described lowering effect of ethanol on LH may be secondary to a direct pituitary locus of action, or involve a metabolic breakdown product of ethanol rather than ethanol itself.

Animals↗
PubMed1999

Ethanol production from renewable resources.

Vast amounts of renewable biomass are available for conversion to liquid fuel, ethanol. In order to convert biomass to ethanol, the efficient utilization of both cellulose-derived and hemicellulose-derived carbohydrates is essential. Six-carbon sugars are readily utilized for this purpose. Pentoses, on the other hand, are more difficult to convert. Several metabolic factors limit the efficient utilization of pentoses (xylose and arabinose). Recent developments in the improvement of microbial cultures provide the versatility of conversion of both hexoses and pentoses to ethanol more efficiently. In addition, novel bioprocess technologies offer a promising prospective for the efficient conversion of biomass and recovery of ethanol.

Biomass↗
PubMed1985

Ethanol drug interaction with chlordiazepoxide and pentobarbital.

Drug interactions between ethanol and pentobarbital and ethanol and chlordiazepoxide were investigated utilizing mice. At the peak of oral ethanol (0-4 g/kg), either sodium pentobarbital (1-120 mg/kg) or chlordiazepoxide hydrochloride (2-400 mg/kg) was given intraperitoneally. Blood concentrations of ethanol, pentobarbital, chlordiazepoxide, and its pharmacologically active major metabolites were monitored utilizing either gas chromatography or high performance liquid chromatography. Lethality and loss-of-righting reflex were measured as indexes of behavioral drug interactions. It was evident from the isobolographic plot that the interactions between ethanol and pentobarbital and ethanol and chlordiazepoxide were more than additive. Interaction between ethanol and pentobarbital was greater than that between ethanol and chlordiazepoxide. Furthermore, with increasing ethanol pretreatment the shift in dose-response curves for the loss-of-righting reflex was affected more than the shift in dose-response curves for lethality. Blood concentration monitoring of each drug indicated that the rate of biotransformation of pentobarbital was significantly decreased; sequential biotransformation of chlordiazepoxide was also altered, resulting in a large accumulation of demethylchlordiazepoxide in the blood.

Animals↗