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At least 469 records · Page 26Linked to original sources
PubMed1993

The effects of in utero ethanol administration on the electrophysiological activity of rat nigrostriatal dopaminergic neurons.

Iontophoresis and single-unit extracellular recording techniques were utilized to study the effects of in utero ethanol administration on nigrostriatal dopaminergic (NSDA) neurons in adult rats. Pregnant Sprague-Dawley rats consumed an ethanol-containing liquid diet providing 0%, 17.5%, or 35% ethanol-derived calories (EDC) from gestation day 8 until parturition. A separate group was fed standard rat chow as an ad lib, diet control. The dose-response curves of intravenously administered apomorphine on the spontaneous activity of NSDA neurons were shifted to the right in animals exposed to a liquid diet containing 17.5% or 35% EDC compared to 0% EDC or ad lib. control groups. The responsiveness of NSDA neurons to microiontophoretic application of the D-2 DA receptor agonist, quinpirole, was not altered following in utero ethanol exposure. These results suggest that in utero ethanol exposure may produce a down-regulation in the function of DA receptors distinct from the somatodendritic impulse-regulating D-2 autoreceptors. The firing pattern of NSDA neurons was also found to be altered after in utero ethanol exposure. There was a dissociation between the firing rate and burst activity in neurons that displayed burst-firing patterns in animals with in utero ethanol exposure. These observations agree with biochemical and behavioral studies that in utero ethanol exposure produces a long-lasting effect on the development of electrophysiological and pharmacological characteristics of midbrain DA systems in adulthood.

Animals↗
PubMed2004

Two zebrafish alcohol dehydrogenases share common ancestry with mammalian class I, II, IV, and V alcohol dehydrogenase genes but have distinct functional characteristics.

Ethanol is teratogenic to many vertebrates. We are utilizing zebrafish as a model system to determine whether there is an association between ethanol metabolism and ethanol-mediated developmental toxicity. Here we report the isolation and characterization of two cDNAs encoding zebrafish alcohol dehydrogenases (ADHs). Phylogenetic analysis of these zebrafish ADHs indicates that they share a common ancestor with mammalian class I, II, IV, and V ADHs. The genes encoding these zebrafish ADHs have been named Adh8a and Adh8b by the nomenclature committee. Both genes were genetically mapped to chromosome 13. The 1450-bp Adh8a is 82, 73, 72, and 72% similar at the amino acid level to the Baltic cod ADH8 (previously named ADH1), the human ADH1B2, the mouse ADH1, and the rat ADH1, respectively. Also, the 1484-bp Adh8b is 77, 68, 67, and 66% similar at the amino acid level to the Baltic cod ADH8, the human ADH1B2, the mouse ADH1, and the rat ADH1, respectively. ADH8A and ADH8B share 86% amino acid similarity. To characterize the functional properties of ADH8A and ADH8B, recombinant proteins were purified from SF-9 insect cells. Kinetic studies demonstrate that ADH8A metabolizes ethanol, with a V(max) of 13.4 nmol/min/mg protein, whereas ADH8B does not metabolize ethanol. The ADH8A K(m) for ethanol as a substrate is 0.7 mm. 4-Methyl pyrazole, a classical competitive inhibitor of class I ADH, failed to inhibit ADH8A. ADH8B has the capacity to efficiently biotransform longer chain primary alcohols (>/=5 carbons) and S-hydroxymethlyglutathione, whereas ADH8A does not efficiently metabolize these substrates. Finally, mRNA expression studies indicate that both ADH8A and ADH8B mRNA are expressed during early development and in the adult brain, fin, gill, heart, kidney, muscle, and liver. Together these results indicate that class I-like ADH is conserved in zebrafish, albeit with mixed functional properties.

Alcohol Dehydrogenase↗
PubMed1980

Provoked priapism in sickle cell anemia.

Two patients with sickle cell anemia are reported who developed relative impotence after repeated episodes of priapism. They learned that excessive ethanol ingestion produced an erection and utilized this mechanism to satisfy sexual partners. Hospitalization and transfusion therapy were required for repeated episodes of priapism. Extensive interviews were required in order to learn the sequence of events. This synergistic relationship between ethanol and priapism should be sought in patients with repeated hospitalizations for this complication of sickle cell anemia because it is preventable with appropriate counseling.

Adult↗
PubMed2001

Effect of acamprosate and naltrexone, alone or in combination, on ethanol consumption.

Both acamprosate and naltrexone have demonstrated clinical utility in reducing relapse to alcohol use in recovering alcoholics. The present experiments examined the effects of acamprosate and naltrexone, either alone or in combination, on basal ethanol consumption in a limited-access model with the use of outbred Wistar rats. Naltrexone, 0.1 mg/kg, significantly reduced ethanol consumption as previously reported. Acamprosate, 50 mg/kg, did not significantly reduce ethanol consumption when administered alone and provided no evidence of additive or synergistic effects when combined with naltrexone. Acamprosate, 200 mg/kg, produced a modest reduction in ethanol consumption when administered alone but no evidence of additive or synergistic effects when combined with naltrexone. From these findings, it is suggested that a combination approach of these drugs may not be any more effective than monotherapy.

Acamprosate↗
PubMed2003

A 5-HT1A agonist and a 5-HT2c antagonist reduce social interaction deficit induced by multiple ethanol withdrawals in rats.

RATIONALE: Repeated withdrawals from chronic forced ethanol exposure sensitize animals to withdrawal-induced deficits in social interaction behavior. The deficits in social interaction behavior following withdrawal from continuous ethanol exposure can be reduced following acute treatments with 5-HT(2C) antagonists or 5-HT(1A) agonists. OBJECTIVES: The present study investigated whether prior treatment with these serotonergic agents during early withdrawals in rats subjected to repeated withdrawals from ethanol exposure would ameliorate the social interaction deficits observed following the final withdrawal. METHODS: Sprague-Dawley rats were exposed to three cycles of 5 days forced ethanol (7%, w/v), with 2 days of control diet after the first and second cycles. Drugs were administered IP 4 h after removal of ethanol on the first and second cycles but not the third in one group and 4.5 h after removal of ethanol on the third cycle in another. The social interaction test was performed 5 h after removal of ethanol on the third cycle. Drugs tested included SB-242084, a 5-HT(2C) antagonist; buspirone, a 5-HT(1A) partial agonist; WAY-100635, a 5-HT(1A) antagonist; ketanserin, a 5-HT(2A) antagonist; ritanserin, a mixed 5-HT(2A/2C) antagonist; and Ro-601075, a 5-HT(2C) agonist. RESULTS: Both SB-242084 and buspirone reduced ethanol withdrawal-induced deficits in social interaction when given either acutely 30 min before the test or at 4 h after withdrawal from the first and second cycles. WAY-100635 and ketanserin were completely ineffective regardless of mode of treatment. In contrast, the 5-HT(2C) agonist, Ro-601075, accentuated the withdrawal-induced deficit in social interaction behavior in rats exposed to either 4.5 or 7% ethanol diet. CONCLUSIONS: These results support the utility of 5-HT(1A) agonists and 5-HT(2C) antagonists in reducing anxiety-like behavior induced by ethanol withdrawal and reducing the adaptive changes associated with repeated withdrawals.

Aminopyridines↗
PubMed2005

The influence of different cultivation conditions on the metabolome of Fusarium oxysporum.

The two most widespread pentose sugars found in the biosphere are d-xylose and l-arabinose. They are both potential substrates for ethanol production. The purpose of this study was to better understand the redox constraints imposed to Fusarium oxysporum during utilization of pentoses. In order to increase ethanol yield and decrease by-product formation, nitrate was used as nitrogen source. The use of NADH, the cofactor in denitrification process when using nitrate as a nitrogen source, improved the ethanol yield on xylose to 0.89 mol mol(-1) compared to the ethanol yield achieved using ammonium as nitrogen source 0.44 mol mol(-1). The improved ethanol yield was followed by a 28% decrease in yield of the by-product xylitol. In order to investigate the metabolic pathway of arabinose and the metabolic limitations for the efficient ethanol production from this sugar, the extracellular and intracellular metabolite profiles were determined under aerobic and anaerobic cultivation conditions. The results of this study clearly show difficulties in channelling of glucose-1-P (G1P) to pentose phosphate pathway (PPP) and reduced NADPH regeneration, suggesting that NADPH becomes a limiting factor for arabinose conversion, resulting in excessive acetate production. Variations of the fungus intracellular amino and non-amino acid pool, under different culture conditions, were evaluated using principal component analysis (PCA). PCA projection of the metabolome data collected from F. oxysporum subjected to environmental perturbations succeeded to visualize different physiological states and the conclusions of this study were that the metabolite profile is unique according to: (1) the carbon source and (2) the oxygen supply, and to a lesser extent to the cultivation phase.

Adaptation, Physiological↗
PubMedDate not supplied

[Effect of ethanol on the biosynthesis of major components of triacylglycerols and phospholipids in the rat liver].

Content of triacylglycerols was increased in rat liver tissue after administration of ethanol. Independent studies of biosynthesis of fatty acid and glycerol components of glycerolipids exhibited that 3H-leucine was mainly consumed in synthesis of glycerol moiety of phospholipids and triacylglycerols, whereas 14C-acetate was utilized in synthesis of fatty acids. Ethanol activated most distinctly the synthesis of glycerol moiety as compared with the synthesis of triacylglycerol fatty acids. In rat liver tissue ethanol caused an accumulation of unsaturated and monoenic fatty acids, while the ratio of arachidonic acid in phospholipids was decreased. Synthesis of triacylglycerol fatty acids was activated in presence of ethanol with simultaneous decrease in the rate of the label incorporation into linoleic and arachidonic acids; synthesis of fatty acids was stimulated de novo but the following elongation and desaturation of linoleic acid was inhibited. Ethanol activated more effectively esterification of fatty acids with formation of triacylglycerols as compared with phospholipids. Incorporation of the label into glycerol molecule occurred in response to activation of glycero-glyconeogenesis by ethanol. Acetyl-CoA, derived from 14C-acetate, was mainly used in synthesis of triacylglycerols, diacylglycerols, free cholesterol and its esters. Acetyl-CoA, produced from 3H-leucine, was mostly common involved in synthesis of monoacylglycerols and phospholipids.

Animals↗
PubMedDate not supplied

Quantifying ethanol by high performance liquid chromatography with precolumn enzymatic conversion and derivatization with fluorimetric detection.

We quantified ethanol by measurement of the subsequent increase in acetaldehyde after reaction with alcohol dehydrogenase and nicotinamide adenine dinucleotide (ADH-NAD) with a fluorimetric HPLC method. Ethanol standards ranging from 0.3 to 200 mg/dl were investigated and the limit of quantitation of the fluorimetric HPLC method was found to be 6 mg/dl. The accuracy of the HPLC method was assessed by assaying blood samples containing 6-200 mg/dl of ethanol and comparing its results to those of the ADH-NAD enzymatic method (r2 = 0.993). The coefficients of variation for intraassay (assayed ten times) and interassay (assayed on 7 consecutive days) were 6.7% and 9.3% for blood samples containing 50 mg/dl of ethanol and 4.0% and 17.9% for blood samples containing 200 mg/dl of ethanol. The blood ethanol concentrations of a volunteer after a pulse of 0.3 g/kg of ethanol determined with the described HPLC method were correlated to the results from the ADH-NAD enzymatic method (r2 = 0.986). In conclusion, the fluorimetric HPLC method for measurement of ethanol here described is of potential clinical utility.

Alcohol Dehydrogenase↗
PubMed1996

Comparison of the stimulus properties of ethanol and the Ca2+ channel antagonist nimodipine in rats.

A variety of L-type Ca2+ channel antagonists, including the dihydropyridine derivative nimodipine, have been shown to be effective in reducing ethanol intake and preference in animal models of alcoholism. The behavioral mechanism involved in the anti-alcohol effects of nimodipine are, however, not clear yet. The aim of the present study was to investigate the possibility that the effects of nimodipine on ethanol intake are based on stimulus substitution. Therefore, rats were trained to discriminate ethanol (12.5% w/v, 1000 mg/kg i.p.) from saline in a two-lever food-reinforced drug discrimination procedure (dose range of ethanol tested: 125-1000 mg/kg i.p., ED50 value: 488 mg/kg). In cross-generalization tests with nimodipine (0.15-15 mg/kg i.p.), stimulus substitution was not noted. In addition, a cross-familiarization conditioned taste aversion paradigm was utilized. In rats, 1000 mg/kg i.p. ethanol was used as the reference drug producing a conditioned taste aversion. Effects of preexposure to ethanol (500-1500 mg/kg i.p.) and nimodipine (7.5-30 mg/kg i.p.) on the magnitude of the ethanol-induced conditioned taste aversion were investigated as an index for stimulus similarity between preexposure and reference drug. Preexposure to both ethanol and nimodipine prevented the development of a conditioned taste aversion. Contrary to the drug discrimination results, these latter findings suggest that there may be similarities between the stimulus properties of nimodipine and ethanol. Moreover, the apparent discrepancy between the results obtained in drug discrimination and cross-familiarization conditioned taste aversion suggests that different stimulus properties of ethanol control behavior in both procedures. The finding that, under particular conditions, ethanol and nimodipine appear to share common stimulus properties needs to be further evaluated, as this may be related to the reported anti-alcohol effects of nimodipine and other Ca2+ channel antagonists.

Analysis of Variance↗
PubMed1990

In vitro 31P-NMR spectroscopic studies of rat liver subjected to chronic ethanol administration.

31P-NMR spectroscopy of rat liver perchloric acid extracts was utilized to assess hepatic levels of major phosphorylated metabolites with and without ethanol administration from 0 to 51 days. The results are: (1) 3-phosphoglycerate was largely decreased starting from the first day of ethanol ingestion, (2) in ethanol-treated rats, phosphoethanolamine exhibited a significant decrease relative to the control rats until around day 30, (3) glycerophosphocholine and glycerophosphoethanolamine decreased over the entire period of ethanol ingestion, (4) ATP, AMP, Pi and energy charge showed significant changes due to ethanol effects when a 40-50 s exposure to CO2 was used prior to freeze-clamping, but ADP did not change, and (5) the other observable metabolites did not show statistically significant change. Some time-dependent changes in metabolite concentration, although not dramatic, were observed from day 1 to day 51 of ethanol administration. Our results indicate that chronic ethanol ingestion results in an inhibition of glycolysis and gluconeogenesis, a decrease in phospholipid breakdown and a lowering of hepatic energy charge.

Adenosine Diphosphate↗
PubMed1990

Development of tolerance to ethanol in cultured adrenal chromaffin cells.

Dissociated bovine adrenal chromaffin cells in culture were utilized to study the mechanisms for development of cellular tolerance to ethanol. Three days after plating, cells were grown in either control medium or medium containing 200 mM ethanol for periods up to 6 days. Catecholamine release induced by carbachol, 80 mM K+, BAY K 8644, and veratrine was studied in ethanol-treated and untreated cultures. The presence of ethanol in vitro was inhibitory to all these stimuli in untreated cell cultures, carbachol-induced release being most sensitive (IC50 approximately 30 mM). After growth in ethanol for 6 days, carbachol-induced catecholamine release was completely resistant to the inhibitory effects of ethanol. The resistance to ethanol of carbachol-induced catecholamine release from cells grown in medium containing ethanol also extended to the inhibitory effects of butanol. The results show some similarities with changes observed in the central nervous system during the development of ethanol tolerance, and it is suggested that this model system may be useful in examining the mechanisms by which tolerance occurs.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Ethanol attenuates the response of locus coeruleus neurons to excitatory amino acid agonists in vivo.

Recent in vitro electrophysiological studies have revealed that ethanol specifically reduces N-methyl-D-aspartate (NMDA)-activated ion currents, e.g. in hippocampal slices. In the present study, utilizing extracellular recording techniques, the effect of ethanol on excitatory amino acid induced excitability of rat locus coeruleus noradrenergic neurons was investigated in vivo. Administration of ethanol (2 g/kg, i.p.) significantly inhibited the excitation of the locus coeruleus neurons as produced by microiontophoretic application of glutamate, NMDA or quisqualate, but not that of kainate. In contrast, the locus coeruleus response to similarly applied acetylcholine was unaffected by the ethanol treatment. Although ethanol did not alter the basal firing rate of locus coeruleus neurons, the drug significantly changed the firing pattern of the neurons into a more regularized rhythm. It is proposed that the presently observed attenuation of glutamate excitation of locus coeruleus by ethanol may constitute part of the underlaying mechanism for ethanol intoxication in man.

Acetylcholine↗
PubMed1983

Metabolism of fensulfothion by a soil bacterium, Pseudomonas alcaligenes C1.

Fensulfothion (O,O-diethyl O-[4-(methylsulfinyl)phenyl]phosphorothioate), an organophosphorus pesticide used to control the golden nematode Heterodera rostochiensis, is used as a source of carbon by microorganisms isolated from soils treated with the pesticide. Two of the microbial isolates, Pseudomonas alcaligenes C1 and Alcaligenes sp. strain NC3, used more than 80% of the pesticide in 120 h in culture when supplemented as a source of carbon. P. alcaligenes C1, which showed maximal growth on fensulfothion, degraded the compound to p-methylsulfinyl phenol and diethyl phosphorothioic acid. The phenolic metabolite could be identified by conventional spectral analysis, whereas the spectral patterns of the phosphorus-containing metabolite suggested that the compound was complexed with some cellular molecules. However, utilization of the phosphoric acid ester and ethanol by P. alcaligenes C1 suggested that the microbe attacks fensulfothion by an initial hydrolysis of the compound and subsequent utilization of the phosphoric acid ester. The pathway of degradation of fensulfothion by P. alcaligenes is of great value in the detoxification of the pesticide residues and also in the environmentally stable phosphoric acid esters.

Biodegradation, Environmental↗
PubMed2005

Numerical and genetic analysis of polycyclic aromatic hydrocarbon-degrading mycobacteria.

Ability to degrade high molecular weight polycyclic aromatic hydrocarbons (PAHs) has been found in diverse species of fast-growing mycobacteria. This study included several PAH-degrading mycobacteria from heavily contaminated sites and an uncontaminated humus soil in the Natural Park, Schwäbische Alb, Germany. The numerical analysis with a total of 131 tests showed that isolates from humus soil and contaminated sites had similar substrate utilization patterns for primary alcohols from ethanol to pentanol, 1,4-butanediol, benzyl alcohol, hexadecane, ethyl acetate, fluoranthene, phenanthrene, and pyrene as the sole carbon and energy (C/E) sources. Significant differences between the two subgroups isolated from humus soil and contaminated sites were observed in the utilization of polyalcoholic sugars, including adonitol, D: -arabitol, L: -arabitol, erythritol, inositol, rhamnose, sorbitol, and xylitol. Among isolates from humus soil, strain PYR100 showed high similarity in 16S rDNA sequence with M. vanbaalenii strain PYR-1 (=DSM 7251, 100%) and M. austroafricanum ATCC 33464 (99.9%). In addition to the numerical analysis, the 16S-23S intergenic spacer sequence was useful for discriminating between the closely related strains PYR100 and PYR-1 (98% similarity). The patterns of the variable V2 and V3 regions in the ribosomal RNA gene corresponding to Escherichia coli positions 179 to 197 and 1006 to 1023, respectively, were useful for dividing fast-growing and thermosensitive PAH-degrading mycobacteria into ten subgroups consistent with the phylogenetic positions.

Base Sequence↗
PubMed2005

In vitro co-metabolism of acetoacetate and ethanol in human hepatic mitochondrial and cytosolic fractions.

The rate of alcohol elimination is highly resistant to acceleration in vivo in well-nourished individuals. The acceleration of ethanol elimination may be achieved by providing the conditions in which the action of alcohol dehydrogenase is not delayed by the insufficiency of the oxidized NAD form. The aim of the study was to verify the theoretically assumed mechanism of accelerating alcohol elimination by administering excessive acetoacetate (Ac-Ac) in the experimental in vitro model. Ac-Ac forming the redox system with beta-hydroxybutyrate (beta-HBA) is the natural acceptor of excessive protons from ethanol oxidation. Ac-Ac and beta-HBA penetrate freely through the cell membranes and are easily assimilated energetic substrates. The examinations were performed using the hepatic homogenates (collected from the cadavers shortly after death) supplemented with ethanol and Ac-Ac. The ethanol levels were determined at 0, 15, 60, 90 and 150 min of the experiment. The findings showed that the equimolar addition of Ac-Ac resulted in a two- to three-fold increase in ethanol oxidation in hepatic homogenates. The biochemical system discussed above resembles the natural way of utilizing the excessive NADH, which is formed during ethanol combustion in chronic alcoholics. The results indicate that further investigations are necessary to assess the clinical importance of this metabolic system.

Acetoacetates↗
PubMed1988

Effects of acute ethanol administration on the hepatic xanthine dehydrogenase/oxidase system in the rat.

Administration of ethanol (5 g/kg p.o.) to female Sprague-Dawley rats resulted in conversion of a portion of hepatic xanthine dehydrogenase to xanthine oxidase 12 hr after treatment. Conversion was partly reversed in vitro by treatment of hepatic 100,000 X g supernatant with dithiothreitol, whereas pretreatment of rats with pyrazole (100 mg/kg i.p.) prevented conversion 18 hr after ethanol administration. Incubation of acetaldehyde with rat liver supernatant at 37 degrees C converted xanthine dehydrogenase to xanthine oxidase in a dose-dependent manner, whereas incubation of ethanol with rat liver supernatant did not lead to conversion. Acetaldehyde-induced conversion in vitro was reversed by treatment with dithiothreitol, and was partially blocked by addition of equimolar concentrations of reduced glutathione. These data suggest that biotransformation of ethanol is required for conversion of hepatic xanthine dehydrogenase to xanthine oxidase. Because xanthine oxidase utilizes molecular oxygen to produce superoxide radical, ethanol-induced conversion of xanthine dehydrogenase to xanthine oxidase could contribute to the enhanced lipid peroxidation reported previously after administration of a single dose of ethanol.

Acetaldehyde↗
PubMed1993

Electrophoretically mediated microanalysis of ethanol.

Capillary electrophoresis was used to determine ethanol by the methodology of electrophoretically mediated microanalysis (EMMA). In EMMA, spatially distinct analyte and analytical reagent zones of differing electrophoretic mobility are merged under the influence of an electric field, and the resulting product is transported to the detector. The enzymatic oxidation of ethanol to acetaldehyde by alcohol dehydrogenase was utilized, and the concurrent reduction of NAD+ to NADH was monitored at 340 nm as a measure of the quantity of ethanol injected. Quantitation using an internal standard and normalization for peak migration time yielded a R.S.D. of 2.7%, and the linear range extended to that quantity of ethanol which could be reacted prior to passing by the detection window. Comparison of the EMMA technique to the Sigma spectrophotometric procedure revealed that the two methods do not yield significantly different values for the determination of ethanol. The EMMA method offered the advantages of electrophoretic mixing and miniaturization.

Acetaldehyde↗