Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ethanol utilization”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed2005

Substrate-binding in quinoprotein ethanol dehydrogenase from pseudomonas aeruginosa studied by electron paramagnetic resonance at 94 GHz.

Pyrroloquinoline quinone (2,7,9-tricarboxypyrroloquinoline quinone, PQQ) is one of several quinone cofactors that is utilized in a class of dehydrogenases known as quinoproteins. In this contribution, we have used continuous-wave high-field/high-frequency electron paramagnetic resonance (EPR) at 94 GHz (W-band) to study substrate binding in ethanol dehydrogenase (QEDH) from Pseudomonas aeruginosa, taking advantage of the fact that the enzyme is isolated with a substantial proportion of the PQQ cofactor in the paramagnetic semiquinone form. In the substrate-free enzyme, the principal values of the g-tensor, obtained by spectral simulation are: gx = 2.00585(2), gy = 2.00518(2), and gz = 2.00212(2), giving giso = 2.00438(2). All three principal values of the g-tensor decrease when ethanol is bound to the protein: gx = 2.00574(2), gy = 2.00511(2), and gz = 2.00207(2), giving giso = 2.00431(2). The results represent the first direct evidence for the tight binding of an alcohol to a PQQ-dependent alcohol dehydrogenase and show that ethanol also binds to the enzyme even when the PQQ cofactor is in the semiquinone form. The decrease in g is consistent with an increase in polarity in the immediate vicinity of the PQQ cofactor and probably reflects a changed geometry of the PQQ-Ca2+ complex when ethanol binds.

Alcohol Oxidoreductases↗
PubMed1976

Inhibitory effects of H2 on growth of Clostridium cellobioparum.

Hydrogen inhibits the growth of hydrogen-producing Clostridium cellobioparum, but not of Escherichia coli or Bacteroides ruminicola. The inhibition is reversible. When hydrogen was removed either by palladium black or by gassing out the tube, glucose utilization increased as did optical density and hydrogen production of C. cellobioparum. Removal of the H2 by methanogenic bacteria favors the growth of C. cellobioparum. Grown with Methanobacterium ruminantium in various concentrations of glucose, the Clostridium reaches a higher optical density and produces more H2 and a higher viable cell count. The cell yield is also higher than in pure culture. In mixed culture, C. cellobioparum produces more acetic acid and less lactic acid, ethanol, and butyric acid than in pure culture. The significance of this metabolic shift and hydrogen utilization in methanogenesis is discussed.

Animals↗
PubMed1995

Divergent modes of autophagy in the methylotrophic yeast Pichia pastoris.

The budding yeast Pichia pastoris responds to methanolic media by synthesizing high levels of cytosolic enzymes (e.g. formate dehydrogenase) and peroxisomal enzymes (e.g. alcohol oxidase), which are necessary to assimilate this carbon source. Major alterations in cellular metabolism are initiated upon a shift in carbon source to ethanol or glucose. These alterations require the synthesis of new proteins and the rapid degradation of those enzymes no longer needed for methanol utilization. In this study, we have measured cytosolic and peroxisomal enzyme activities and examined the fate of morphologically distinct peroxisomes to assess the degradative response of this yeast during nutrient adaptation. Utilizing biochemical, morphological and genetic approaches, we have shown that there exist in P. pastoris at least two pathways for the sequestration of peroxisomes into the vacuole for degradation. The ethanol-induced pathway is independent of protein synthesis and includes an intermediate stage in which individual peroxisomes are sequestered into autophagosomes by wrapping membranes, which then fuse with the vacuole. This process is analogous to macroautophagy. The glucose-induced pathway invokes the engulfment of clusters of peroxisomes by finger-like protrusions of the vacuole by a process analogous to microautophagy. Unlike ethanol adaptation, glucose stimulated the degradation of formate dehydrogenase as well. Peroxisomes remained outside the vacuoles of glucose-adapted cycloheximide-treated normal cells, suggesting that protein synthesis is required for peroxisome entry into the yeast vacuole. Two complementary mutants (gsa1 and gsa2) that are unable to degrade peroxisomes or formate dehydrogenase during glucose adaptation were isolated. The mutated gene products appear to function in one or more events upstream of degradation within the vacuole, since ethanol-induced peroxisome degradation proceeded normally in these mutants and peroxisomes were found outside the vacuoles of glucose-adapted gsa2 cells. Mutants lacking vacuolar proteinases A and B were unable to degrade alcohol oxidase or formate dehydrogenase during ethanol or glucose adaptation. Peroxisomes were found to accumulate within the vacuoles of these proteinase mutants during adaptation. Combined, the results suggest that there exist in Pichia pastoris two independent pathways for the sequestration of peroxisomes into the vacuole, the site of degradation.

Alcohol Oxidoreductases↗
PubMed1998

Phospholipase D activity is required for suppression of yeast phosphatidylinositol transfer protein defects.

Yeast phosphatidylinositol transfer protein (Sec14p) function is essential for production of Golgi-derived secretory vesicles, and this requirement is bypassed by mutations in at least seven genes. Analyses of such 'bypass Sec14p' mutants suggest that Sec14p acts to maintain an essential Golgi membrane diacylglycerol (DAG) pool that somehow acts to promote Golgi secretory function. SPO14 encodes the sole yeast phosphatidylinositol-4,5-bisphosphate-activated phospholipase D (PLD). PLD function, while essential for meiosis, is dispensable for vegetative growth. Herein, we report specific physiological circumstances under which an unanticipated requirement for PLD activity in yeast vegetative Golgi secretory function is revealed. This PLD involvement is essential in 'bypass Sec14p' mutants where normally Sec14p-dependent Golgi secretory reactions are occurring in a Sec14p-independent manner. PLD catalytic activity is necessary but not sufficient for 'bypass Sec14p', and yeast operating under 'bypass Sec14p' conditions are ethanol-sensitive. These data suggest that PLD supports 'bypass Sec14p' by generating a phosphatidic acid pool that is somehow utilized in supporting yeast Golgi secretory function.

Carrier Proteins↗
PubMed1988

The influence of ethanol on hepatic transmethylation.

One of the most important biochemical pathways in the organism is the biosynthesis of methionine from the methylation of homocysteine. Two different reactions are responsible for this methylation, one utilizing N5-methyltetra-hydrofolate as a methylating agent and the other using betaine as the methyl donor. This paper reviews some recent findings in this laboratory, which demonstrate that ethanol-feeding to rats impairs the folate-induced reaction. Our findings also show that this impairment is compensated for through the adaptive increase in the enzyme using betaine in the biosynthesis of methionine. Further studies indicate that the mechanism of action in the impairment may occur through the formation of individual adducts between the folate-induced enzyme (methionine synthetase), its essential cofactors and acetaldehyde, a metabolic product of ethanol. These findings suggest a basis for why rats are more resistant to alcoholic liver injury than humans and may offer a means of protecting against alcoholic liver injury in man.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1987

The effect of activity state upon the production of lethalities due to the inhalation of the toxic pyrolysis products of polyacrylonitrile.

Hydrogen cyanide is known to be produced upon the pyrolysis of the synthetic material polyacrylonitrile. Cyanide inhibits phosphorylation reactions, therefore, decreasing the amount of high energy bonds available for metabolic use. Since the energy requirements, as well as the respiratory minute volume, for an individual decrease with decreasing activity, it was of interest to investigate whether diminished physical activity would decrease the lethal potential of the pyrolysis products of polyacrylonitrile. In order to produce wide variations in physical activity, male ICR mice were pretreated with either 8.6 mg/kg dextroamphetamine sulfate ip 30 min prior to challenge, 75 mg/kg sodium pentobarbital ip 15 min prior to challenge, or 10 ml/kg of 70 proof ethyl alcohol ip 15 min prior to challenge. Control animals received injections of 10 ml/kg normal saline ip 15 min prior to challenge. Animals were subsequently challenged with the cooled/filtered smoke from the pyrolysis of polyacrylonitrile fibers at 660 C. Increased physical activity decreased the exposure time necessary to produce death. Animals pretreated with amphetamine appear to die more rapidly than control animals due to an increase in respiratory minute volume. Animals pretreated with sodium pentobarbital or ethanol appear to survive through long periods of exposure to the toxic gases due to both a decrease in minute volume and a decrease in energy utilization.

Acrylic Resins↗
PubMed1975

Effect of ethanol on phospholipid metabolism by the rat lung.

Prefeeding of alcohol shows the in vivo incorporation of orally administered palmitic acid into phosphatidylcholine of the lung. This impairment is also demonstrable in vitro utilizing lung slices and 14C-labeled palmitate or cytidine 5'-diphosphocholine as precursors. It is concluded that alcohol ingestion affects the utilization of precursors needed for phospholipid formation in the lung.

Animals↗
PubMed1966

Effects of prolonged ingestion of glucose or ethanol on tissue lipid composition and lipid biosynthesis in rat.

The effects on lipid metabolism of long-term feeding of large amounts of ethanol or glucose differed from those that have been reported in short-term experiments. Three groups of male rats were investigated. The first was fed lab chow and 15% (v/v) ethanol ad lib.; the second was pair-fed with the first and given isocaloric amounts of glucose in lieu of ethanol; the third was fed lab chow and water ad lib. All three groups consumed nearly the same number of calories, and about 30% of the calories in the first group were derived from ethanol. Neither glucose nor ethanol added to a nutritionally adequate diet promoted the development of a fatty liver, although both stimulated acetate-(14)C utilization for hepatic lipid synthesis. In all three groups more than 80% of the label in hepatic lipid was found in fatty acids, and the distribution of label amongst the fatty acids of different chain lengths was virtually the same. Ethanol decreased while glucose increased the quantity of lipid in fat depots, and each altered the fatty acid composition of the lipids in adipose tissue, kidney, liver, and hepatic subcellular fractions in a different manner. The most striking of these changes was the relative increase in monounsaturated fatty acids and the decrease in essential fatty acids produced by glucose.

Acetates↗
PubMed2006

Chronic binge ethanol consumption accelerates progression of simian immunodeficiency virus disease.

BACKGROUND: While alcohol consumption is known to increase the incidence and severity of infections, the impact of alcohol consumption on human immunodeficiency virus (HIV) disease progression has been difficult to assess. Therefore, we examined the effect of ethanol on simian immunodeficiency virus (SIV) disease progression in a well-defined model utilizing rhesus macaques. METHODS: Alcohol was administered for 5 hours via an indwelling intragastric catheter to achieve an alcohol concentration of 50 to 60 mM for 4 consecutive days per week for the duration of the study. Control animals received isocaloric sucrose. After 3 months, animals were inoculated intravenously with 10,000 times the ID(50) of SIV(DeltaB670) and followed to end-stage disease. RESULTS: Plasma SIV ribonucleic acid (RNA) was higher in alcohol-consuming animals compared with sucrose-treated animals during the early asymptomatic stage of disease but not at later time points. This increase in viral set point was associated with more rapid progression to end-stage disease in macaques administered alcohol (median=374 days) compared with sucrose (median=900 days). The decline in blood CD4+ cells was similar in both groups of animals. CONCLUSIONS: This study indicates that frequent episodes of alcohol intoxication in SIV+ macaques increase viral set point in association with more rapid development of end-stage disease.

Alcohol Drinking↗
PubMed1986

Hydroxylation of acetone by ethanol- and acetone-inducible cytochrome P-450 in liver microsomes and reconstituted membranes.

Acetone oxidation in rat liver microsomes was induced 5- or 8-fold by the treatment of the animals with ethanol or acetone, respectively. The apparent Km of the reaction was 0.9 mM, a value lower than the concentration reported for plasma acetone under starvation conditions. The major acetone metabolite was identified as acetol by GC-MS. Acetone oxidation in microsomes was inhibited by typical P-450 inhibitors as well as by compounds (e.g. imidazole) known to interact with the ethanol-inducible P-450 form. Antibodies against this P-450 isozyme were inhibitory for the reaction in rabbit liver microsomes and this isozyme was the only one that showed acetone hydroxylation activity in reconstituted membranes. Imidazole inhibited the conversion of [14C]acetone into low-Mr compounds (e.g. glucose) in vivo. It is suggested that the ethanol- and acetone-inducible P-450 make use of acetone as an endogenous substrate in the utilization of the compound for, e.g. glucose production under conditions of starvation and diabetic ketoacidosis.

Acetone↗
PubMed2006

In vivo antidiabetic and antioxidant potential of Helichrysum plicatum ssp. plicatum capitulums in streptozotocin-induced-diabetic rats.

Helichrysum species (Asteraceae) are widely found in Anatolia. Decoction prepared from the capitulums of Helichrysum plicatum ssp. plicatum is used to alleviate the symptoms of diabetes mellitus in folk medicine. In the present study, the hypoglycaemic and antioxidant potential of Helichrysum plicatum ssp. plicatum was evaluated by using in vivo methods in normal and streptozotocin-induced-diabetic rats. After the oral administration of water and ethanolic extracts at doses of 500mg/kg body weight prepared from the capitulums of plant, blood glucose levels were monitored at specific intervals. Tolbutamide was used as a reference drug at a dose of 100mg/kg. The experimental data indicated that water and ethanol extracts of capitulums demonstrate significant antihyperglycaemic and antioxidant activity in streptozotocin-induced rats which confirmed the folkloric utilization. In order to assess the role of polyphenolic components in the relevant activity, phenolic and flavonoid contents of each extract were also determined in terms of total phenols: 113.5+/-8.6mg (gallic acid equivalent/1g extract) and total flavanoids 50.5+/-1.9mg (quercetin equivalent/1g extract) for ethanol extract, total phenols: 75.9+/-3.7, flavonoids: 31.5+/-2.3 for water extract using Folin-Ciocalteu reagent.

Animals↗
PubMedDate not supplied

Metabolic state of the rat liver with ethanol: comparison of in vivo 31phosphorus nuclear magnetic resonance spectroscopy with freeze clamp assessment.

In vivo 31phosphorus nuclear magnetic resonance spectroscopy was used to measure the hepatic metabolic state in various groups of rats given ethanol, a control liquid diet or a solid chow diet. The use of selective presaturation pulses applied to the broad phosphorus resonances of immobile phospholipids permitted reliable determination of ATP/ADP ratios by quantitation of the ATP-beta and ATP-gamma peak areas. ATP/ADP ratios were depressed by both techniques in rats chronically ingesting ethanol compared to pair-fed animals consuming the control liquid diet. These differences were observed regardless of whether ethanol feeding was continued up to the time of investigation or whether it was discontinued for 24 hr prior to study. Acute alcohol administration in chow-fed rats, not previously ingesting ethanol, did not lower hepatic ATP/ADP ratios by either methodology. In all cases, liver ATP/ADP ratios assessed by 31phosphorus nuclear magnetic resonance spectroscopy were higher than those measured by high-performance liquid chromatography. However, parallel decreases in hepatic ATP/ADP ratios were observed with chronic ethanol consumption by both 31phosphorus nuclear magnetic resonance spectroscopy and the biochemical method, confirming the utility of in vivo 31phosphorus nuclear magnetic resonance spectroscopy for assessment of the hepatic bioenergetic status. The difference in absolute ATP/ADP ratios by the two methods may to some degree be explained by binding effects of ADP with proteins or mitochondrial membranes, rendering it partially invisible to nuclear magnetic resonance or alternatively, by breakdown of high energy phosphate bonds with freeze clamp extraction.

Adenosine Diphosphate↗
PubMed1995

Acute prenatal ethanol exposure and luteinizing hormone-releasing hormone messenger RNA expression in the fetal mouse brain.

Ethanol exposure during critical periods of development results in alterations of central nervous system morphology and function. In this study, the effects of acute ethanol exposure on the number of neurons expressing luteinizing hormone-releasing hormone (LHRH) messenger RNA (mRNA) has been analyzed. Also, the expression of LHRH mRNA in the diagonal band of Broca/preoptic area (DBB/POA) was determined. Pregnant C57BL/6J mice were intubated with two doses of a 25% solution of ethanol or water (2.9 g/kg body weight) 4 hr apart on gestation day 7 (G7), G10, or G11. Animals were killed on G18, and in situ hybridization was utilized to detect neurons expressing LHRH mRNA. The number of neurons expressing LHRH mRNA was determined along their migration route from the rostrum into the forebrain. Ethanol exposure on G7 did not significantly change the number of neurons expressing LHRH mRNA on G18 compared with that in control animals. However, the number of neurons expressing LHRH mRNA in the nasal septum area in animals exposed to ethanol on G10 or G11 was significantly less than the number in control animals (p < 0.05). Prenatal ethanol exposure on any of the aforementioned treatment days did not alter the expression of LHRH mRNA at the level of the DBB/POA on G18 in ethanol-treated animals compared with control animals. Also, neuron-specific enolase mRNA expression at the level of the DBB/POA was not altered by prenatal ethanol exposure. Therefore, ethanol exposure on the aforementioned treatment days did not differentially affect LHRH mRNA expression compared with neuron-specific enolase mRNA expression at the level of the DBB/POA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1997

Cytochrome P-4502E1: its physiological and pathological role.

The role of the microsomal ethanol-oxidizing system (MEOS) in hepatic ethanol metabolism is reviewed, with focus on its constitutive, ethanol-inducible cytochrome P-4502E1 (2E1). The MEOS was purified and reconstituted using 2E1, phospholipids, and cytochrome P-450 reductase and shown to oxidize ethanol to acetaldehyde, mainly as a monooxygenase and secondarily via hydroxyl radicals, with transcriptional and posttranscriptional regulation. Polymorphism of 2E1 was recognized, and enzymology (including cofactors, role of lipids, inducers, and inhibitors) as well as cellular and tissue distribution were chartered. Physiological functions involve lipid metabolism and ketone utilization in starvation, obesity, and diabetes. The most significant role of 2E1 is its adaptive response to high blood ethanol levels with a corresponding acceleration of ethanol metabolism. The associated free radical production, however, contributes to liver injury in the alcoholic. Most importantly, 2E1 has a unique capacity to activate many xenobiotics (85 of which are listed) to hepatotoxic or carcinogenic products. Induction of 2E1 also results in enhanced production of acetaldehyde, a highly reactive and toxic metabolite. The proliferation of the endoplasmic reticulum associated with 2E1 induction is also accompanied by enhanced activity of other cytochrome P-450s, resulting in accelerated metabolism of, and tolerance to, other drugs, as well as increased degradation of retinol and its hepatic depletion. Some substrates and metabolites, however, are innocuous and may eventually be used as markers of heavy drinking. Recently discovered effective 2E1 inhibitors also have great therapeutic potential.

Animals↗
PubMedDate not supplied

Prenatal ethanol effects on NGF level, NPY and ChAT immunoreactivity in mouse entorhinal cortex: a preliminary study.

It has been reported that maternal ethanol consumption leads to deficits in the limbic areas involved in cognitive functions and interferes with synthesis and utilization of neurotrophins. In the present study, it was hypothesized that prenatal alcohol intake might induce neuroanatomical alterations in the entorhinal cortex (EC). We also investigated the possible EC involvement of brain nerve growth factor (NGF), the first neurotrophin to be isolated, during such pathological events. To test this hypothesis, we used pregnant mice exposed to ethanol during EC neurogenesis (starting about gestational day 8). Our data show that prenatal alcohol intake in male mice alters the EC neuronal growth and differentiation. These morphological alterations are accompanied by an altered NGF level in the EC of prenatal alcohol-treated mice. We also found a decrease in choline acetyltransferase- and neuropeptide Y-immunopositive neurons in the EC of alcohol-exposed mice. However, the relationship between neuronal damage induced in the EC by ethanol, low presence of NGF, and the possible functional and behavioral consequences remains to be elucidated.

Animals↗