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PubMed1989

Ethanol administration diminishes the endotoxin-induced increase in glucose metabolism.

The metabolism of ethanol (ETOH) is known to increase the cytosolic NADH/NAD ratio and consequently impairs hepatic glucose output in the fasted state. In contrast, one of the characteristic alterations in glucose metabolism produced by the administration of endotoxin is an increase in the de novo synthesis of glucose. Therefore, the present study tests the hypothesis that the acute administration of ETOH will prevent the endotoxin-induced increase in glucose production. In vivo glucose kinetics were determined by the infusion of [6-3H, U-14C]glucose in catheterized conscious rats. The intravenous infusion of tracer glucose, and ETOH (100 mg/100 g b.w./hr) or saline were started at the same time and both continued throughout the experiment. Two hours later the ETOH infusion rate was decreased to maintain the blood ETOH levels between 100 and 160 mg/dl. At 140 min, endotoxin (100 micrograms/100 g b.w.) was injected. ETOH alone did not alter basal values of plasma glucose (5 mM), glucose rate of appearance (Ra; 35 mumols/min/kg) or metabolic clearance (MCR; 7 ml/min/kg). Endotoxin alone increased plasma glucose (80%) and lactate (140%) concentrations, glucose Ra (60%) and recycling (40%) in saline-infused rats, whereas in ETOH-infused animals, plasma glucose and lactate levels were only elevated 40% and glucose Ra and recycling were unchanged. The results show that acute ETOH administration diminishes the increased glucose production and utilization seen in endotoxemia. The attenuation of the endotoxin effect by ethanol is due to inhibition of hepatic glucose production and peripheral glucose utilization.

Animals↗

PubMed1994

Influence of age on the development of rapid tolerance to ethanol.

Fischer-344 rats of three different ages (4, 13, and 25 months) were tested to determine the extent and duration of rapid tolerance to ethanol-induced hypothermia and hypnosis. There were no significant differences among groups with regard to maximal ethanol hypothermia (3.0-3.5 g/kg ethanol), nor did any of the groups display a significant change (rapid tolerance) in the maximal hypothermic response when tested with a second identical challenge 48 h later. Rapid tolerance to ethanol hypnosis was observed across groups at 48 h, utilizing two different dosing schemes. No tolerance was observed if 14 days were allowed to elapse between the initial and the test challenge. Young rats were observed to develop a greater degree of rapid tolerance than did middle-aged or old rats, using hypnosis as a measure.

Aging↗

PubMed1996

An alternative column chromatographic process for the production of human albumin.

We have modified a standard column chromatography method for the preparation of albumin from human plasma. The proposed method utilizes Sephadex G-25, euglobulin precipitation, DEAE-Sepharose, ethanol heat treatment and Sephacryl S-200 HR. The procedure differs from that normally used by the introduction of Schneider's ethanol/heat treatment step and the elimination of a CM-Sepharose step, after the DEAE-Sepharose step. The proposed method was used to produce 15 batches of albumin, 100 liters of plasma per batch. Purity of more than 99% was obtained at an average yield of 26.5 g/l plasma for the albumin produced. All batches presented 99.2 to 99.9% monomer and 0.1 to 0.8% dimer, with no larger polymers detected. The utilization of the final gel filtration step eliminated highly polymerized albumin usually obtained during the process. The advantages of the proposed method are reduction in the overall process time from 6 to 5 days, elimination of the CM-Sepharose step and the reduction of 6 to 4 columns in series for the Sephacryl S-200 HR step.

Chemical Fractionation↗

PubMed2005

Ethanolic fermentation of acid pre-treated starch industry effluents by recombinant Saccharomyces cerevisiae strains.

Two industrial effluents, a pre-fermentation effluent and a post-fermentation effluent from a wheat starch production plant, were used as substrates for fuel ethanol production in anaerobic batch cultures using minimal nutritional amendment. The performances of three metabolically engineered xylose-utilizing Saccharomyces cerevisiae strains: TMB 3001 expressing XYL1, XYL2 and XKS1, redox metabolism modulated CPB.CR1 and glucose de-repressed CPB.CR2, as well as a reference strain CEN.PK 113-7D not fermenting xylose, were evaluated. For the recombinant strains a glucose consumption phase preceded the xylose consumption phase. In both effluents, biomass and ethanol production occurred predominantly during the glucose consumption phase, whereas xylitol and glycerol formation were predominant in the xylose consumption phase. Total specific ethanol productivities on glucose were 6-fold higher than on xylose in the pre-fermentation effluent and 15-fold higher than on xylose in the post-fermentation effluent. CPB.CR1 showed impaired growth compared to the two other xylose-utilizing strains, but displayed 18% increased ethanol yield in the post-fermentation effluent.

Biomass↗

PubMed2001

On the diagnosis of hypoglycemia in car drivers--including a review of the literature.

Hypoglycemia may reach forensic relevance concerning the psychophysical ability of running a car and with respect to a possible imputability. Our retrospective study included anamnesis and clinical symptoms observed in drivers with impaired performance to point out correlations between biochemical parameters and the actual course of the disease and its sequelae on roadworthiness. Clinical-biochemical estimations were performed on glucose, lactic acid and ethanol including a toxicological screening. It is proposed to utilize the estimation of glucose and lactic acid (the so-called combined value) in blood samples taken on behalf of the police as an important hint to the actual state of glucose metabolism. The anamnesis and the symptomatology may complete the biochemical analyses.

Accidents, Traffic↗

PubMed2005

Fed-batch cultivation of Mucor indicus in dilute-acid lignocellulosic hydrolyzate for ethanol production.

Mucor indicus fermented dilute-acid lignocellulosic hydrolyzates to ethanol in fed-batch cultivation with complete hexose utilization and partial uptake of xylose. The fungus was tolerant to the inhibitors present in the hydrolyzates. It grew in media containing furfural (1 g/l), hydroxymethylfurfural (1 g/l), vanillin (1 g/l), or acetic acid (7 g/l), but did not germinate directly in the hydrolyzate. However, with fed-batch methodology, after initial growth of M. indicus in 500 ml enzymatic wheat hydrolyzate, lignocellulosic hydrolyzate was fermented with feeding rates 55 and 100 ml/h. The fungus consumed more than 46% of the initial xylose, while less than half of this xylose was excreted in the form of xylitol. The ethanol yield was 0.43 g/g total consumed sugar, and reached the maximum concentration of 19.6 g ethanol/l at the end of feeding phase. Filamentous growth, which is regarded as the main obstacle to large-scale cultivation of M. indicus, was avoided in the fed-batch experiments.

Acetic Acid↗

PubMed1988

Effect of chronic ethanol administration on iron metabolism in the rat.

This study shows that the ingestion of ethanol provokes alterations in iron metabolism which may lead to iron overload. Impaired release of reticuloendothelial iron was shown by a decrease of the maximum red blood cell utilization when radioactive iron was supplied as colloidal iron. An impairment in the erythropoietic activity of ethanol-treated animals was also observed, as can be seen from the reduced plasma iron turnover and red blood cell utilization within 24 h of iron administration. A rise in marrow transit time was also observed. In ethanol-treated rats there was an increase in the amount of iron retained both in the liver and the spleen. This was observed in both sexes and also in the offspring from ethanol-treated mothers.

Animals↗

PubMed1998

The combined effects of chronic ethanol/desipramine treatment on beta-adrenoceptor density and coupling efficiency in rat brain.

Both ethanol and desipramine influence beta-adrenoceptor regulation. We reported previously that ethanol partially counteracted desipramine's effects on beta-adrenoceptor. Previous studies utilized beta-adrenoceptor radioligands that also bind to 5-HT1B receptors, thus, changes in 5-HT1B receptors could have confounded the results. The effects of chronic ethanol, desipramine and ethanol/desipramine treatment on beta-adrenoceptor coupling efficiency to Gs protein in rat brain were examined using 125I-iodocyanopindolol after blocking binding to 5-HT1B receptors. In the frontal cortex, ethanol uncoupled beta-adrenoceptor from GS. Desipramine decreased beta-adrenoceptor density, particularly in the high-conformational state, with no effect on coupling. In combined treatment, desipramine prevented ethanol-induced uncoupling. In the hippocampus, desipramine enhanced beta-adrenoceptor coupling, but ethanol had no effect. In combination with desipramine, ethanol enhanced desipramine-induced decrease in beta-adrenoceptor density in the high-conformational state, but uncoupled beta-adrenoceptors, an effect not observed with ethanol alone. These results suggest a complex interplay between ethanol and antidepressants in modulating beta-adrenoceptor function.

Adrenergic Uptake Inhibitors↗

PubMed1979

Effects of ethanol on plasma protein shedding in the human stomach.

Plasma protein shedding in the stomach was measured in 23 normal individuals before and after intragastric administration of a 30% solution of ethyl alcohol. Two different methods were used to assess plasma protein shedding. The first technique utilizes [131I]albumin and requires neutralization of the gastric juice. It was used in 12 subjects and failed to demonstrate any increase of plasma protein shedding under the influence of ethanol. The second technique which utilizes [51Cr]chloride was used in 11 subjects. It demonstrated a significant increase of the gastric clearance of plasma protein which reached 2.5 times the control values. The [51Cr]chloride technique does not require prior neutralization of gastric acidity. It is concluded that, in normal man, ethanol administration increases plasma protein shedding in the stomach when it is given in the presence of an acid gastric juice. The effect is not observed when the gastric acidity is neutralized.

Adult↗

PubMed1996

Fermentation and Sulfur Reduction in the Mat-Building Cyanobacterium Microcoleus chthonoplastes.

The mat-building cyanobacterium Microcoleus chthonoplastes carried out a mixed-acid fermentation when incubated under anoxic conditions in the dark. Endogenous storage carbohydrate was fermented to acetate, ethanol, formate, lactate, H(inf2), and CO(inf2). Cells with a low glycogen content (about 0.3 (mu)mol of glucose per mg of protein) produced acetate and ethanol in equimolar amounts. In addition to glycogen, part of the osmoprotectant, glucosyl-glycerol, was degraded. The glucose component of glucosyl-glycerol was fermented, whereas glycerol was released into the medium. Cells with a high content of glycogen (about 2 (mu)mol of glucose per mg of protein) did not utilize glucosyl-glycerol. These cells produced more acetate than ethanol. M. chthonoplastes was also capable of using elemental sulfur as the electron acceptor during fermentation, resulting in the production of sulfide. With sulfur present, acetate production increased whereas ethanol production decreased. Also, less formate was produced and the evolution of hydrogen ceased completely. In general, the carbon recoveries were satisfactory but the oxidation-reduction balances were too high. The latter could be explained by assuming the reduction of ferric iron, which is associated with the cells, mediated by the oxidation of formate. The switch from photoautotrophic to fermentative metabolism did not require de novo protein synthesis, and fermentation started immediately upon transfer to dark anoxic conditions. From the molar ratios of the fermentation products and from measurement of enzyme activities in cell extracts, we concluded that glucose derived from glycogen and glucosyl-glycerol is degraded via the Embden-Meyerhof-Parnas pathway.

Journal Article↗

PubMed1996

Alcohol and glucose metabolism in skeletal muscles in the rat.

Ethanol is known to cause an acute and profound insulin resistance in man and the rat primarily via effects on glucose utilization. This paper examines the nature of these inhibitory effects on whole-body glucose utilization using the euglycaemic hyperinsulinaemic clamp in the conscious unrestrained rat. We confirm that ethanol infusion causes an acute insulin resistance, the rate of glucose infusion required to maintain euglycaemia (GIR) being decreased markedly by ethanol. To ensure that the GIR is a measure of whole-body glucose disposal, glucose turnover and hepatic glycogen levels were measured. These studies showed that ethanol totally suppressed hepatic glucose production. The reduction in GIR is associated with marked decreases in glucose uptake and glycogen synthesis in most skeletal muscles. In oxidative but not in non-oxidative muscles, the activation of glycogen synthase in response to insulin was decreased by ethanol, suggesting that a defect in glycogen synthase activation may be responsible for the decrease in glycogen synthesis. The basis of the inhibitory effects of ethanol on insulin-stimulated glucose metabolism in muscle is unknown, but may involve membrane-associated impairments in insulin signalling and/or the glucose transport system.

Journal Article↗

PubMed1989

Physiological Properties of a Mutant of Pachysolen tannophilus Deficient in NADPH-Dependent d-Xylose Reductase.

A d-xylose reductase mutant of Pachysolen tannophilus was isolated on the basis of its poor growth on d-xylose but normal growth on xylitol and d-glucose. Fractionation of cell extracts indicated that the mutant was deficient in d-xylose reductase activity that used NADPH exclusively as a cofactor, but not in activity that used both NADH and NADPH. Mutant cultures grown on d-xylose as the sole carbon source exhibited some properties that would be desired in improved strains. Growth rate, growth yield, and d-xylose consumption rate of the mutant were less sensitive than those of the wild type to changes in aeration rate. d-Xylose was utilized more efficiently in that less of a by-product, xylitol, was produced. In addition, under low aeration conditions, more ethanol was produced. A disadvantage was a relatively slow rate of d-xylose utilization.

Journal Article↗

PubMed1988

Structure and regulation of the ethanol-inducible cytochrome P450j.

Specific polyclonal antisera against microsomal ethanol-inducible cytochrome P450 (P450j, P450IIE) were prepared and utilized to isolate cDNA for P450j from lambda gt11 cDNA libraries. The longest cDNAs encoding P450j of rat and human were completely sequenced. The rat P450j sequence was compared to those of other P450s (P450II gene family members) to determine the structural similarity. Southern-blot analysis of rat and human genomic DNAs verified that only a single gene shared extensive homology with P450j. Cloned P450j cDNA and antibodies were used to study the expression of P450j gene during development and by various inducers as well as in pathological conditions. By combination of cDNA hybridization and immunoblot analyses, three types of P450j gene expression were observed: transcriptional activation during development; post-transcriptional activation (probably via protein stabilization) by various inducers such as pyrazole, 4-methylpyrazole, acetone, and ethanol; and mRNA stabilization in diabetic and starved animals. These three different types of P450j induction appeared to be present not only in liver but also in lung and kidney tissues.

Animals↗

PubMed1993

High-frequency (35-70 kHz) ultrasonic vocalizations in rats confronted with anesthetized conspecifics: effects of gepirone, ethanol, and diazepam.

The effects of three anxiolytics--gepirone, diazepam, and ethanol--on high-frequency ultrasonic vocalizations elicited from rats via a new method are described. Subjects confronted with an anesthetized, same-sex conspecific in a neutral test cage emitted ultrasonic vocalizations in the 35- to 70-kHz range. The great majority of these were calls with frequencies higher than 40 kHz; of these, short calls (< 50 ms) occurred significantly more frequently than long calls (> 50 ms). Female subjects emitted far more of these high-short and high-long vocalizations than males did. In females, but not males, these calls were reduced in number by gepirone, 5-hydroxytryptamine1A (5-HT1A) agonist, at both 1.0- and 10.0-mg/kg doses and by diazepam, a benzodiazepine, at 3.0 but not 1.0 mg/kg. Ethanol (0.6 and 1.2 g/kg) had no detectable effect. The utility of this method, both for the study of ultrasounds and assessment of serotonergic anxiolytics, is discussed.

Anesthetics↗

PubMed1996

Neurochemical bases of locomotion and ethanol stimulant effects.

The locomotor stimulant effect produced by alcohol (ethanol) is one of a large number of measurable ethanol effects. Ethanol-induced euphoria in humans and locomotor stimulation in rodents, a potential animal model of human euphoria, have long been recognized and the latter has been extensively characterized. Since the euphoria produced by ethanol may influence the development of uncontrolled or excessive alcohol use, a solid understanding of the neurochemical substrates underlying such effects is important. Such an understanding for spontaneous locomotion and for ethanol's stimulant effects is beginning to emerge. Herein we review what is known about three neurochemical substrates of locomotion and of ethanol's locomotor stimulant effects. Several lines of research have implicated dopaminergic, GABAergic, and glutamatergic neurotransmitter systems in determining these behaviors. A large collection of work is cited, which strongly implicates the above-mentioned neurotransmitter substances in the control of spontaneous locomotion. A smaller, but persuasive, body of evidence suggests that central nervous system processes utilizing these transmitters are involved in determining the effects of ethanol on locomotion. Particular emphasis has been placed on the mesolimbic ventral tegmental area to nucleus accumbens dopaminergic pathway, and on the ventral pallidum/substantia innominata, where GABA and glutamate have been found to play a role in altering the activity of this dopaminergic pathway. Research on ethanol and drug locomotor sensitization, increased responsiveness to the substance with repeated administration, is also reviewed as a process that may be important in the development of drug addiction.

Animals↗

PubMed1989

Differences in susceptibility of rat liver and brain sialidases to ethanol and gangliosides.

Based on reports that ethanol can decrease the level of sialic acid (SA) (neuraminic acid) in several tissues, we tested the hypothesis that ethanol promotes SA cleavage by enhancing the activity of sialidases (neuraminidases). We also investigated whether brain and liver sialidases have the same response to ethanol and gangliosides, especially since our prior studies have demonstrated that gangliosides could antagonize ethanol-induced behavior. Experiments were conducted on homogenates of brain and liver and of liver slices of adult rats. In liver slices, cleavage of SA did not fall in proportion to the ethanol-induced inhibition of sialidase; in fact, at 0.1 M ethanol, free SA increased, even though sialidase was inhibited. Brain sialidase activity on endogenous sialoglycoconjugates was much more resistant to ethanol than liver sialidase and was fully active even in concentrations as high as 1 M. When gangliosides were incubated with liver slices in the absence of ethanol, sialidase was markedly stimulated. The ethanol-induced inhibition of sialdase in liver slices was mimicked by sorbitol, suggesting that the inhibition may be caused by a shift in redox state as a result of increased NADH. The ethanol metabolite, acetaldehyde, does not seem to be a factor, because sialidase inhibition still occurred when slices were incubated with ethanol containing pyrazole. The results indicate that ethanol promotes the accumulation of free SA in liver without stimulating sialdase; our other work suggests that the cause is an increase in accessibility to sialoglycoconjugates rather than decreased utilization of SA. Brain and liver sialidases clearly respond differently to both ethanol and gangliosides.

Animals↗

PubMed2000

Amelioration of ethanol-induced neurotoxicity in the neonatal rat central nervous system by antioxidant therapy.

BACKGROUND: The cerebellum of the neonatal rat is highly susceptible to ethanol, with profound loss of Purkinje cells resulting from even brief exposure during the first postnatal week. Developmental ethanol exposure previously has been shown to induce free radicals/oxidative stress processes and/or down-regulate protective antioxidants. In an earlier study, we found antioxidants protected against ethanol neurotoxicity in a tissue culture environment. The present study was designed to determine whether similar protection could be manifested in the intact animal. METHODS: Neonatal rats were administered a liquid diet via intragastric intubation on postnatal days 4 and 5 (P4-P5), the peak period of ethanol sensitivity in the developing cerebellum. The diet consisted of milk formula with 12% ethanol, the isocaloric substitution of maltose-dextrin for ethanol, or ethanol plus the antioxidant vitamin E. Unbiased three-dimensional counting was utilized to analyze Purkinje cell numbers and density within defined volumes from these animals on P5. RESULTS: These determinations revealed a substantial loss of Purkinje cells in the ethanol-treated animals compared to controls (approximately 30-44%), but this loss was prevented by the inclusion of vitamin E (601U/100 ml) in the diet. A lower concentration of the antioxidant (301U/100 ml) was not effective in this regard, however. CONCLUSIONS: These results suggest that ethanol-related cerebellar damage during this early postnatal period may be related to oxidative stress processes or the insufficiency of protective antioxidants. Thus, antioxidant treatment may represent a possible therapy for preventing or ameliorating the central nervous system (CNS) damage seen in the fetal alcohol syndrome.

Animals↗

PubMed2006

Comparison of blood ethanol concentrations in samples simultaneously collected into expired and unexpired venipuncture tubes.

Blood sample collection kits manufactured for the Minnesota Bureau of Criminal Apprehension contain venipuncture tubes with an expiration date that the tube manufacturer utilizes to ensure sufficient vacuum to fill the tubes. Legal challenges to blood ethanol analyses that involved the use of expired venipuncture tubes prompted a study comparing ethanol analysis results in expired venipuncture tubes (up to 74 months beyond the expiration date) and in unexpired venipuncture tubes. Blood samples were collected during controlled drinking sessions using 10-mL venipuncture tubes containing 100 mg of sodium fluoride and 20 mg of potassium oxalate and were analyzed by headspace gas chromatography. The data obtained indicate that the ethanol concentrations in the expired and unexpired venipuncture tubes were statistically identical.

Blood Specimen Collection↗