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PubMed1992

Selection of strains capable of utilizing D-xylose and cellobiose to produce ethanol by electric field-induced protoplast fusion.

The protoplast fusion between Candida guilliermondii S208 (Arg-) and Saccharomyces cerevisiae 314 was induced by three pulses (18kV/cm, 10 microseconds duration) applied at an interval of 1 s with the model GH-401 Electric Induced Gene Transfer/Cell Fusion System. The frequency of appearance of prototrophic hybrids was 3.6 x 10(-3). Stable fusion products were obtained after continual subculture over 20 times on selected and unselected media. Comparative studies showed that the fusion products were real hybrids of both parents. Two fustants, F-106 and F-308, could ferment both D-xylose and cellobiose to ethanol. The ethanol production of F-106 in the media containing 2% D-xylose or 2% cellobiose were 3.1g/l and 1.05g/l, respectively. The ethanol production of F-308 in the above media were 0.2g/l and 2.8g/l, respectively.

Candida↗
PubMed2005

Utilizing the urinary 5-HTOL/5-HIAA ratio to determine ethanol origin in civil aviation accident victims.

Specimens from fatal aviation accident victims are submitted to the FAA Civil Aerospace Medical Institute for toxicological analysis. During toxicological evaluations, ethanol analysis is performed on all cases. Care must be taken when interpreting a positive ethanol result due to the potential for postmortem ethanol formation. Several indicators of postmortem ethanol formation exist; however, none are completely reliable. The consumption of ethanol has been shown to alter the concentration of two major serotonin metabolites, 5-hydroxytryptophol (5-HTOL) and 5-hydroxyindole-3-acetic acid (5-HIAA). While the 5-HTOL/5-HIAA ratio is normally very low, previous studies using living subjects have demonstrated that the urinary 5-HTOL/5-HIAA ratio is significantly elevated for 11-19 h after acute ethanol ingestion. Recently, our laboratory developed and validated an analytical method for the simultaneous determination of both 5-HTOL and 5-HIAA in forensic urine samples using a simple liquid/liquid extraction and LC/MS/MS and LC/MS/MS/MS. In this previous work a 15 pmol/nmol serotonin metabolite ratio cutoff was established in postmortem urine, below which it could be conclusively determined that no recent antemortem ethanol consumption had occurred. In the current study this newly validated analytical method was applied to five ethanol-positive aviation fatalities where the origin of the ethanol present could not previously be conclusively determined. In four of the five cases examined the detected ethanol was demonstrated to be present due to postmortem microbial formation, and not consumption, even though some indication of ethanol consumption may have been present.

Accidents, Aviation↗
PubMed1977

Ethanol-host interactions determined by radiorespirometry of 14C glucoses.

1. Theoretical considerations in continuous flow analysis by Walker, Shepherdson and McGowan have been applied to continuous flow radiorespirometry of 14C-glucoses to demonstrate ethanol response differences between water- and ethanol preferring mice. 2. Ethanol dosages in the n mols/kg range stimulated glucose utilization rates more in ethanol-than in water-preferring mice, while intermediate dosages (micron and low mmol/kg) produced equal stimulation but at different dosages. Pharmacological dosages (20-88 mmols/kg) inhibited glucose rates in water-preferring mice. The inhibition was released at 44 mmols/kg in ethanol-preferring mice. 3. Inhibition release was shown to be associated more with glucose carbons other than one, and considered consistent with a sodium-plus potassium-activated ATPase mechanism. 4. Intermediate ethanol dosage changes could be assigned to differences induced in glucose carbon one metabolism with H2O2-catalase and/or microsomal-ethanol-oxidizing systems (MEOS) mechanisms. 5. Our studies suggest that measurements of adenylate deaminase activities might clarify shifts in transaminations (human) and shifts in mononucleotides seen following chronic ethanol ingestion.

Acetates↗
PubMed2004

Ethanol and illicit drugs do not affect the diagnostic utility of base deficit and lactate in differentiating minor from major injury in trauma patients.

OBJECTIVES: Base deficit (BD) and lactate are valuable screening tools for injured patients. They reflect the degree of oxygen debt and have been shown to predict outcome. Intake of ethanol and illicit drugs may further derange acid-base status. The authors evaluated the effect of blood alcohol level (BAL) and illicit drugs on admission BD and lactate levels in trauma patients. METHODS: Prospective, observational study of trauma patients in a Level 1 trauma center. Patients with penetrating or blunt trauma were included in the study. Patients were further stratified into major or minor categories. Major was defined by an Injury Severity Score >15, blood transfusions, or a decrease in hematocrit of more than ten points. Injury categories were further divided into several subgroups based on presence or absence of ethanol (BAL > or =0.08 g/dL) or positive urine toxicology screen (Utox). RESULTS: A total of 520 patients (84% male) with a mean (+/-SD) age of 33 (+/-15) years were studied. Compared with the minor injury categories, BD and lactate levels were significantly higher in the major injury categories in all different intoxication subgroups. Testing the diagnostic performance of BD and lactate in detecting major injury, the authors observed significant (p < 0.05) differences between the areas under the receiver operating characteristic curves for these two diagnostic tests compared with baseline in both intoxicated (BAL > or =0.08 g/dL and/or positive Utox) and nonintoxicated (BAL <0.08 g/dL and negative Utox) patients. CONCLUSIONS: The presence of ethanol and/or illicit drugs did not affect the ability of BD or lactate to identify patients with major injuries.

Acid-Base Imbalance↗
PubMedDate not supplied

Effect of ethanol on brain catecholamines in rat lines developed for differential ethanol-induced motor impairment.

The importance of the central catecholamines, with the emphasis on the noradrenergic neurons in the differential sensitivity to ethanol between the AT (alcohol-tolerant) rats selected for low and the ANT (alcohol-nontolerant) rats selected for high sensitivity to ethanol-induced (2 g/kg) motor impairment, was clarified by studying the effects of ethanol (2 and 4 g/kg, IP) on the utilization of norepinephrine (NA) and dopamine (DA), and on the metabolism of NA. The utilization of the catecholamines was estimated from the disappearance of the amines after inhibition of the brain tyrosine hydroxylase by alpha-methyl-p-tyrosine (200 mg/kg, IP), given 15 min after the administration of ethanol. The formation of 3-methoxy-4-hydroxy-phenylglycol (MHPG) was used as an estimate of NA metabolism, and was measured 30 min after the administration of ethanol. The basal utilization rate of NA and DA was similar between the two rat lines, but the increased formation of MHPG suggested that the naive AT rats had a higher noradrenergic activity in the limbic forebrain, hypothalamus, and cerebellum than did ANT rats. In the brain of both lines, ethanol accelerated the utilization and metabolism of NA in the same manner. Ethanol also increased the utilization of DA in the limbic forebrain of the AT and ANT rats. The higher sensitivity of the ANT rats' DA neurons to ethanol in the limbic forebrain and striatum was revealed by the significant rat line X ethanol interaction. The present findings suggest that the AT and ANT rats differ in the dopaminergic, but not in the noradrenergic responses to ethanol.

Animals↗
PubMed2004

Ethanol-mediated variations in cellular fatty acid composition and protein profiles of two genotypically different strains of Escherichia coli O157:H7.

Two strains of Escherichia coli O157:H7 were grown in tryptic soy broth (TSB, pH 7.1) supplemented with 0, 2.5, 5.0, 7.5, and 10% ethanol at 30 degrees C for up to 54 h. Growth rates in TSB supplemented with 0, 2.5, and 5.0% ethanol decreased with an increase in ethanol concentration. Growth was not observed in TSB supplemented with 7.5 or 10% ethanol. The pH of TSB containing 5.0% ethanol decreased to 5.8 within 12 h and then increased to 7.0 at 54 h. The ethanol content in TSB supplemented with 2.5 or 5.0% ethanol did not change substantially during the first 36 h of incubation but decreased slightly thereafter, indicating utilization or degradation of ethanol by both strains. Glucose was depleted in TSB supplemented with 0, 2.5, or 5.0% ethanol within 12 h. Cells grown under ethanol stress contained a higher amount of fatty acids. With the exceptions of cis-oleic acid and nonadecanoic acid, larger amounts of fatty acid were present in stationary-phase cells of the two strains grown in TSB supplemented with 5.0% ethanol for 30 h than in cells grown in TSB without ethanol for 22 h. The trans-oleic acid content was 10-fold higher in the cells grown in TSB with 5.0% ethanol than those grown in TSB without ethanol. In contrast, cis-oleic acid was not detected in ethanol-stressed cells but was present at concentrations of 0.32 and 0.36 mg/g of cells of the two strains grown in TSB without ethanol. Protein content was higher in ethanol-stressed cells than in nonstressed cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis protein profiles varied qualitatively as affected by the strain and the presence of ethanol in TSB. An ethanol-mediated protein (28 kDa) was observed in the ethanol-stressed cells but not in control cells. It is concluded that the two test strains of E. coli O157:H7 underwent phenotypic modifications in cellular fatty acid composition and protein profiles in response to ethanol stress. The potential for cross protection against subsequent stresses applied in food preservation technologies as a result of these changes is under investigation.

DNA, Bacterial↗
PubMed1971

Glucose-lactate interrelationships: effect of ethanol.

The effect of ethanol on the interrelationship of lactate and glucose metabolism was investigated in eight human volunteers. Lactate and glucose kinetics and intervconversion rates were determined by the sequential administration of L-(+) lactate-U-(14)C and glucose-1-(14)C over an 8 hr period. After a 12 hr fast, the glucose turnover and recycling rates were 94.0 +/-3.8 (SEM) and 13.7 +/-1.1 mg/kg per hr, respectively. Approximately 50% of the glucose turnover or 40.7 +/-2.1 mg/kg per hr was converted to lactate, accounting for 50% of the lactate turnover rate. Lactate turnover and lactate conversion to glucose were 81.8 +/-6.2 and 16.7 +/-1.1 mg/kg per hr, respectively. Approximately 20% of the glucose turnover was derived from lactate under these conditions. During the administration of ethanol, the blood lactate concentration doubled and the lactate turnover rate declined slightly. Lactate conversion to glucose was markedly inhibited, decreasing from 16 to 5 mg/kg per hr, and the per cent of the glucose turnover derived from lactate decreased from 18 to 6. Despite the marked inhibition of lactate conversion to glucose, neither the blood glucose concentration nor the glucose turnover rate changed. Both glucose recycling and glucose conversion to lactate were decreased, indicating that ethanol inhibited peripheral glucose utilization. There was no difference in the degree of inhibition of lactate incorporation into glucose produced by ethanol when nonfasted subjects were compared with two subjects who had fasted for 48-72 hr despite the presence of hypoglycemia in the latter. These results indicate that starvation is not a prerequisite for ethanol inhibition of gluconeogenesis from lactate in humans but is necessary for the development of hypoglycemia. Inhibition of lactate incorporation into glucose in nonfasted subjects is probably masked by a concomitant increase in glycogenolysis which prevents hypoglycemia. Ethanol decreases glucose conversion to lactate as well as lactate conversion to glucose, thus inhibiting the Cori cycle.

Adult↗
PubMedDate not supplied

Diet composition, alcohol utilization, and dependence.

Experiments were carried out in which a nutritionally balanced liquid diet previously used in this laboratory was modified as to total calorie content and high or low carbohydrate and fat concentration. Ethanol was added at 4.5% and 6.2% of diet weight and provided either 27% or 34-37% of total calories depending upon the changes in nutrient content. Measurements included 8-day food/calorie and ethanol consumption, plasma ethanol level, liver alcohol dehydrogenase (ADH) activity, and rate of audiogenic-induced withdrawal seizures. The original liquid diet with 4.5% ethanol was consumed in significantly lesser amounts than the alcohol-free diet, and essentially no body weight gain occurred, regardless if the major nonalcohol, nonprotein calorie source was fat or carbohydrate. When the calorie content of the diet was boosted through the addition of extra carbohydrate or fat (at the expense of water), appreciable weight gain was noted; in the case of the higher calorie diet boosted with more carbohydrate (maltodextrin) calories, growth was similar to that observed on the alcohol-free control diet. On this latter diet ethanol calories appeared to be utilized close to their theoretical value of 7 kcal/g. Blood alcohol levels were significantly higher on the lower calorie diets and were lowest on the high-calorie, high-carbohydrate, 4.5% ethanol diet. This diet also allowed for the lowest rate of withdrawal seizures despite an ethanol intake that was as high as on the lower calorie diets. Essentially, no differences were noted among ADH activities for the dietary treatments studied and thus, did not explain the differences observed among blood ethanol levels. When the alcohol concentration in the high-carbohydrate, high-calorie diet was raised to 6.2% from 4.5% to provide 34% of total calories, the rats responded by decreasing their food (and alcohol) intake to the same level as did the animals receiving a much lower calorie diet, but with 37% of caloric alcohol content. This suggests that at a diet alcohol concentration of 34-37%, one or more nutrient metabolites become limiting in the utilization of ethanol, resulting in food intake adjustments that maintain similar amounts of alcohol consumption.

Alcohol Drinking↗
PubMed1987

Comparison of the effects of ethanol and 4-methylpyrazole on the pharmacokinetics and toxicity of ethylene glycol in the dog.

The purpose of this investigation was to compare the effects of ethanol and 4-methylpyrazole (4MP) on the toxicity and pharmacokinetics of ethylene glycol (EG) in the dog. All dogs received 173 mmol/kg EG, p.o. Dogs were randomly assigned to 3 groups: EG-treated only, EG + ethanol (19.3 mmol/kg, i.v. 3, 7, 14 and 24 h after EG) and EG + 4MP (0.24 mmol/kg, i.v. 3 h after EG, 0.18 mmol/kg at 24 h and 0.06 mmol/kg at 36 h). EG produced a rapid onset of metabolic acidosis (within 3 h) and acute oliguric renal failure (after 48 h), whereas administration of ethanol or 4MP greatly attenuated acidosis and prevented renal toxicity. The administration of ethanol, however, severely increased the central nervous system (CNS) depression that existed after ingestion of EG. The half-life of FG in serum was 10.8 +/- 0.7 h in the EG-only treatment group, 6.8 +/- 0.7 (P less than 0.05) in the EG + ethanol group and 9.8 +/- 0.9 h in the EG + 4MP group. Approx. 10% and 48% of the dose of EG was excreted unchanged in the urine at the 0-3 and 3-72 h periods, respectively. Treatment with 4MP increased the amount of EG excreted in the urine (71% from 3-72 h), whereas ethanol did not (51%). However, both ethanol and 4MP increased the rate constant of EG excretion into urine approx. 70%. These data demonstrate the utility of 4MP over ethanol for the treatment of EG-induced toxicity in dogs and indicate that ethanol and 4MP cause an increase in the rate constant of EG excretion in the urine and not a prolongation in EG half-life.

Animals↗
PubMed1998

In vivo endotoxin enhances biliary ethanol-dependent free radical generation.

Endotoxemia is associated with alcoholic liver diseases; however, the effect of endotoxin on the oxidation of ethanol is not known. We tested the hypothesis that endotoxin treatment enhances hepatic ethanol radical production. The generation of free radicals by the liver was studied with spin-trapping technique utilizing the primary trap ethanol (0.8 g/kg) and the secondary trap alpha-(4-pyridyl-1-oxide)-N-t-butylnitrone (4-POBN; 500 mg/kg). Electron paramagnetic resonance (EPR) spectra of bile showed six-line signals, which were dependent on ethanol, indicating the trapping of ethanol-dependent radicals. Intravenous injections of Escherichia coli lipopolysaccharide (0.5 mg/kg) 0.5 h before 4-POBN plus ethanol treatment caused threefold increases of biliary radical adducts. EPR analyses of bile from [1-13C]ethanol-treated endotoxic rats showed the presence of species attributable to alpha-hydroxyethyl adduct, carbon-centered adducts, and ascorbate radical. The generation of endotoxin-induced increases of ethanol-dependent radicals was suppressed by 50% on GdCl3 (20 mg/kg i.v.) or desferrioxamine mesylate (1 g/kg i.p.) treatment. Our data show that in vivo endotoxin increases biliary ethanol-dependent free radical formation and that these processes are modulated by Kupffer cell activation and catalytic metals.

Animals↗
PubMed2001

Influence of ethanol on thermoregulation: mapping quantitative trait loci.

The genetic basis for the effects of ethanol on thermoregulation was investigated by utilizing recombinant inbred mouse strains from C57BL/6J and DBA/2J progenitor strains. Changes in core body temperature (T(c)) and the degree of fluctuation of T(c) were monitored in male mice following the administration of ethanol in an environment with cyclic changes in ambient temperature (T(a)). Changes in T(c) were utilized to assess ethanol-induced effects on regulated T(c), whereas fluctuations in T(c) were utilized to assess thermoregulatory disruption. Ethanol was administered intraperitoneally at 1.5, 2.5, and 3.5 g/kg for all strains. Change in T(c) and increase in tail temperature were also evaluated at 2.5 g/kg ethanol in a constant T(a) of 26 degrees C. Associations between the measured physiological responses and previously mapped genetic markers were used to identify quantitative trait loci (QTLs). This established probable chromosome locations for a number of genes for the responses. To our knowledge, this is the first report of QTLs that underlie changes in regulation as well as the disruption of a physiological regulatory system.

Animals↗
PubMed1987

Lipogenesis from ketone bodies in the perfused rat liver: effects of acetate and ethanol.

The interactions between acetate or ethanol metabolism, lipogenesis, and ketone body utilization have been studied in isolated livers from fed rats perfused with 15 mM glucose and 10 mM acetate or ethanol. The contribution of acetate to ketogenesis is constant; on the other hand, the contribution of ethanol to ketogenesis increases with time, presumably because of the accumulation of acetate in the perfusate. Ketogenesis is decreased in the presence of ethanol (but not acetate), while ketone body utilization is not affected by ethanol or acetate. Acetate contributes one third and ethanol contributes one half of the carbon incorporated into fatty acids and 3-beta-hydroxysterols. Only a small fraction (less than 5%) of the incorporation of acetate or ethanol into fatty acids and sterols occurs via transient incorporation into ketone bodies.

Acetates↗
PubMed2001

The impact of fermentative organisms on carbon flow in methanogenic systems under constant low-substrate conditions.

We compared carbon flow under constant low-substrate conditions (below 20 microM glucose in situ) in laboratory-scale glucose-fed methanogenic bioreactors containing two very different microbial communities that removed chemical oxygen demand at similar rates. One community contained approximately equal proportions of spiral and cocci morphologies, while the other community was dominated by cocci. In the former bioreactor, over 50% of the cloned SSU rRNA genes and the most common SSU rDNA terminal restriction fragment corresponded to Spirochaetaceae-related sequences, while in the latter bioreactor over 50% of the cloned SSU rRNA genes and the most common SSU rDNA terminal restriction fragment corresponded to Streptococcus-related sequences. Carbon flow was assessed by measuring 14C-labeled metabolites derived from a feeding of [U-14C]glucose that did not alter the concentration of glucose in the bioreactors. Acetate and ethanol were detected in the Spirochaetaceae-dominated reactor, whereas acetate and propionate were detected in the Streptococcus-dominated reactor. A spirochete isolated from a Spirochaetaceae-dominated reactor fermented glucose to acetate, ethanol, and small amounts of lactate. Maximum substrate utilization assays carried out on fluid from the same reactor indicated that acetate and ethanol were rapidly utilized by this community. These data indicate that an acetate- and ethanol-based food chain was present in the Spirochaetaceae-dominated bioreactor, while the typical acetate- and propionate-based food chain was prevalent in the Streptococcus-dominated bioreactor.

Acetates↗
PubMed1972

Characteristics of S organism isolated from Methanobacillus omelianskii.

Previous work showed that Methanobacillus omelianskii was a mixed culture of an ethanol-oxidizing organism called S organism and a hydrogen-utilizing methane bacterium, strain MOH. S organism grows poorly on ethanol unless a hydrogen-utilizing methanogenic bacterium is included to utilize the H(2) produced during growth. Further studies have shown that, among many substrates tested, only ethanol, n-propanol, n-butanol, isobutanol, n-pentanol, acetaldehyde, oxalacetate, and pyruvate are fermented by S organism, either alone or in combination with Methanobacterium ruminantium. It grew better in pure culture with pyruvate than with alcohols. H(2) gas phase inhibited growth on pyruvate as well as on alcohol. When grown alone on pyruvate, S organism produced mainly acetate, ethanol, and CO(2), in addition to a small amount of H(2). When combined with M. ruminantium, no H(2) and very little ethanol were produced and acetate production was increased. When M. ruminantium was present, electrons from pyruvate oxidation by S organism were channeled almost entirely to H(2) and hence to methane formation rather than ethanol. Also, S organism utilized more pyruvate when grown with M. ruminantium. Attempts to obtain better growth of S organism on ethanol by addition of many possible electron acceptors were unsuccessful. It grew best between 32 and 45 C, had a per cent guanine plus cytosine content of deoxyribonucleic acid bases of 47.27 +/- 0.1, contained no cytochrome, and could be grown on a defined medium with pyruvate as the energy and carbon source and with (NH(4))(2)SO(4) as the main nitrogen source. These and other results suggest that S organism belongs in a new genus, but assignment of a definite taxonomic status should await isolation and characterization of more strains.

Acetates↗
PubMed2001

Insertional mutagenesis in the n-alkane-assimilating yeast Yarrowia lipolytica: generation of tagged mutations in genes involved in hydrophobic substrate utilization.

Tagged mutants affected in the degradation of hydrophobic compounds (HC) were generated by insertion of a zeta-URA3 mutagenesis cassette (MTC) into the genome of a zeta-free and ura3 deletion-containing strain of Yarrowia lipolytica. MTC integration occurred predominantly at random by nonhomologous recombination. A total of 8,600 Ura(+) transformants were tested by replica plating for (i) growth on minimal media with alkanes of different chain lengths (decane, dodecane, and hexadecane), oleic acid, tributyrin, or ethanol as the C source and (ii) colonial defects on different glucose-containing media (YPD, YNBD, and YNBcas). A total of 257 mutants were obtained, of which about 70 were affected in HC degradation, representing different types of non-alkane-utilizing (Alk(-)) mutants (phenotypic classes alkA to alkE) and tributyrin degradation mutants. Among Alk(-) mutants, growth defects depending on the alkane chain length were observed (alkAa to alkAc). Furthermore, mutants defective in yeast-hypha transition and ethanol utilization and selected auxotrophic mutants were isolated. Flanking borders of the integrated MTC were sequenced to identify the disrupted genes. Sequence analysis indicated that the MTC was integrated in the LEU1 locus in N083, a leucine-auxotrophic mutant, in the isocitrate dehydrogenase gene of N156 (alkE leaky), in the thioredoxin reductase gene in N040 (alkAc), and in a peroxine gene (PEX14) in N078 (alkD). This indicates that MTC integration is a powerful tool for generating and analyzing tagged mutants in Y. lipolytica.

Alkanes↗
PubMed1985

Measurement of protein synthetic activity by determination of peptidyl[3H]puromycin formation in liver slices after ethanol administration.

We investigated the utility of [3H]puromycin as an alternate and adjunct precursor to amino acids for measuring protein synthetic activity in rat liver slices. Slices were incubated in the presence of either [3H]puromycin or radiolabeled valine to compare the incorporation of these isotopic precursors into nascent hepatocellular proteins. Compared to liver slices from controls, comparable decreases in the incorporation of both [3H]puromycin and labeled valine were observed in experiments using slices from fasted rats and in slices preincubated with 25 mM ethanol. Radiolabeling of nascent polypeptides with either [3H]puromycin or labeled valine in liver slices from rats fed a liquid diet containing ethanol was also decreased compared to slices from pair-fed control and chow-fed animals. Our results demonstrated the validity of using [3H]puromycin to detect changes in protein synthetic activity under these conditions. The potential advantage of using [3H]puromycin for in vivo studies is discussed.

Alcoholism↗