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PubMed1985

Ethanol decreases glucose utilization in healthy man.

The effect of ethanol on glucose utilization during hyperinsulinemia was studied by the euglycemic clamp technique. Normal subjects were given 1 g ethanol/kg body weight for 210 min (oral priming dose of 0.67 g/kg followed by iv infusion of 0.33 g/kg) or 0.9% saline. Insulin infusion, started 90 min after the beginning of ethanol administration, resulted in a mean plasma insulin concentration of 87 +/- 5 (SEM) mU/liter. Plasma glucose was maintained at 5.2 mmol/liter. The rate of glucose metabolism was 23% lower during ethanol (7.1 +/- 0.1 mg/kg X min) than during the control (9.0 +/- 0.8 mg/kg X min) experiment (P less than 0.001). During hyperinsulinemia blood lactate concentrations rose in the control study but this change was abolished by ethanol. The insulin-induced fall of serum triglyceride levels was also inhibited by ethanol. It is concluded that acute intake of alcohol in moderate doses induces insulin resistance.

Adult↗
PubMed1979

Drosophila alcohol dehydrogenase activity in vitro and in vivo: effects of acetone feeding.

When adult Drosophila are placed on medium containing 0.5% acetone, their level of alcohol dehydrogenase activity drops rapidly. At the same time, the proportion of activity in the various electrophoretic forms of the enzyme shifts; most of the activity becomes localized in what is ordinarily a minor form of the enzyme. Moreover, the loss of enzyme activity occurs in vivo as well, as shown by sensitivity to ethanol poisoning, insensitivity to pentenol treatment, and inability to utilize ethanol as an energy source. These observations are discussed in light of a model advanced for the origin of the multiple forms of alcohol dehydrogenase in Drosophila.

Acetone↗
PubMed1982

Acute effects of ethanol and acetaldehyde on plasma phosphate level.

Oral administration of ethanol in a dose of 65 mmol kg-1 produced marked change of plasma phosphate level in rabbits. Hypophosphataemia was observed for the first 2 h after administration followed by significant increase of plasma phosphate at 5 h. Hypophosphataemia did not appear when ethanol was given to the rabbits pretreated with pyrazole. When animals were injected with disulfiram in advance, the duration of hyperphosphataemia due to ethanol was prolonged. Administration of acetaldehyde at a dose of 1.5 mmol kg-1 produced hyperphosphataemia. In this study, plasma phosphate was not associated with change in calcium level. These results suggest that the hypophosphataemia observed was related to the metabolic process of ethanol utilizing alcohol dehydrogenase, and that acetaldehyde, a metabolite of ethanol, might induce the hyperphosphataemia in the animals.

Acetaldehyde↗
PubMed1994

Temperature regulation in mice during withdrawal from ethanol dependence.

Temperature regulation during withdrawal from ethanol dependence was studied in mice. Dependence was induced utilizing ethanol vapor inhalation combined with injections of pyrazole, an alcohol dehydrogenase inhibitor. One control group received vehicle (0.9% NaCl); another received pyrazole (68.1 mg/kg) in vehicle. During withdrawal, mice were placed in a thermal gradient, with core temperature (Tc) and preferred temperature (Tpref) continuously recorded for 26 h. During the period of maximal withdrawal severity (4-10 h after removal from ethanol vapor), the withdrawal group was more active than controls. Withdrawal group Tc [36.4 +/- 0.1 (SE) degrees C] was similar to that of NaCl (36.2 +/- 0.1 degrees C) and pyrazole (36.3 +/- 0.2 degrees C) controls. Withdrawal group Tpref (30.5 +/- 0.5 degrees C) was significantly lower than either NaCl (33.5 +/- 0.3 degrees C) or pyrazole (32.9 +/- 0.5 degrees C) controls. Analysis of covariance with activity as covariate indicated that the difference between Tc and Tpref was greater for the withdrawal group and was due to more than increased activity. Mice withdrawing at constant temperature (29.5 degrees C) did not show Tc different from that of controls. These results support the conclusion that regulated body temperature is not altered during withdrawal. We propose that the lower Tpref of withdrawing mice represents a means of dissipating excess heat that is partly generated by the hypermetabolic state accompanying withdrawal from ethanol dependence.

Alcoholism↗
PubMed1987

Changes in local cerebral glucose utilization after chronic ethanol in rats.

Local rates of cerebral glucose utilization were investigated in ethanol-treated rats using the 2-deoxy[14C]glucose method. Rats received ethanol in drinking water for 3 h each day. After 4 days of exposure to 2 or 4% ethanol (v/v), there was a general tendency toward increased local cerebral glucose utilization. In contrast, after 28 days of exposure to concentrations to 10% ethanol a general depression of cerebral glucose metabolism was observed. Brain regions showing significantly reduced glucose utilization rates in the 28-day group included components of the extrapyramidal system, several thalamic and hypothalamic nuclei, and forebrain limbic structures. A group of animals tested 7 days after discontinuation of ethanol showed essentially normal rates of local cerebral glucose utilization, indicating that alterations in regional brain glucose metabolism induced by this particular regimen and duration of ethanol administration were largely reversible.

Alcoholism↗
PubMed1988

The effects of a choline deficiency on the lipid composition and ethanol tolerance of Drosophila melanogaster.

1. A reduction in the dietary concentration of choline, an essential nutrient for Drosophila melanogaster, from the optimal concentration of 80 micrograms/ml of defined medium to 8 micrograms/ml diminished the level of tissue phosphatidylcholine to less than one-third the normal level in third instar larvae without significantly altering the amount of phosphatidylethanolamine. 2. The rates of synthesis of phospholipids, triglycerides, diglycerides and monoglycerides were reduced by the choline-deficiency, and the chain length of fatty acids in lipids was shortened. 3. The activity of succinic dehydrogenase, a mitochondrial enzyme, was decreased by the deficiency, but the activities of fumarase, sn-glycerol-3-phosphate dehydrogenase, alcohol dehydrogenase, sn-glycerol-3-phosphate oxidase and fatty acid synthetase were unaffected. A choline-deficiency did not alter the ultrastructure of mitochondria of larval fat body cells. 4. Choline-deficient individuals were more susceptible to the toxic effects of ethanol during larval and pupal development, and less adept at utilizing ethanol as a substrate for adult tissue synthesis.

Animals↗
PubMed2004

A laboratory yeast strain suitable for spirit production.

Yeast strains of the species Saccharomyces cerevisiae currently in use for the production of consumable alcohols such as beer, wine and spirits are genetically largely undefined. This prevents the use of standard genetic manipulations, such as crossings and tetrad analysis, for strain improvement. Furthermore, it complicates the application of the majority of modern methods developed in yeast molecular biology. Here we used two haploid laboratory strains with suitable auxotrophic markers for the construction of a genetically well defined, prototrophic diploid production strain. This strain was tested for its fermentative and sensory performances in comparison to commercially available yeasts. Three different fruit mashes (cherries, plums and pears) were fermented in a 90 kg scale. These were then subjected to distillation and used for the production of spirits with a final ethanol content of 40% (v/v). Fermentation parameters assayed included growth, sugar utilization, ethanol production and generation of volatile compounds, higher alcohols and glycerol. The spirits were also tested for their sensory performances and the data obtained statistically consolidated. Our results clearly demonstrate that this laboratory strain does not display any disadvantage compared with commercial yeasts in spirit production for any of the parameters tested, yet it offers the potential to apply both classical breeding and modern molecular genetic techniques for adjusting yeast physiology to special production schemes.

Alcoholic Beverages↗
PubMedDate not supplied

Stereotactic injection of DTI-015 into recurrent malignant gliomas: phase I/II trial.

DTI-015 (BCNU in 100% ethanol) utilizes solvent facilitated perfusion for the intratumoral treatment of gliomas. The ethanol solvent vehicle facilitates a rapid and thorough saturation of the tumor with the dissolved anticancer agent BCNU. We conducted a phase I/II dose escalation study of DTI-015 in 40 heavily pretreated patients with inoperable recurrent malignant glioma. The study goals were to establish a maximally tolerated dose (MTD) for DTI-015 and assess its safety and activity. Patients received stereotactic intratumoral injection of DTI-015 under magnetic resonance imaging guidance. Dose escalation was performed in two phases. First, DTI-015 volume was escalated at a set BCNU concentration of 12.5 mg/ml; second, BCNU mg dose was escalated by increasing BCNU concentration to 30, 45, 60, and 75 mg/ml. A MTD of 5 ml and 240 mg was established. Twenty-five of 28 DTI-015 treatments (89%) using </=MTD were administered safely without producing high-grade drug-related adverse events. Median survival for GBM patients administered DTI-015 at </=MTD was 55 weeks. Magnetic resonance imaging demonstrated stable disease in 72% of evaluable patients with a median of 10.5 weeks. The results suggest that DTI-015 administered at </=MTD is well tolerated and active in patients with inoperable recurrent GBM.

Adult↗
PubMed2003

[Organic acids conversion in methanogenic-phase reactor of the two-phase anaerobic process].

Experiments on organic acids conversion in methanogenic-phase of the two-phase anaerobic process were conducted. The results showed that when the acidogenic-phase was in mixed acids fermentation and its load was 41.5 kg/(m3-d), the load of methanogenic-phase was 6.05 kg/(m3.d), the substrate conversion velocity of bacteria inhabited at the same height of UASB reactor as follows: acetic acid > ethanol > butyric acid > propionic acid; ethanol-utilized microbial had the same pH range as methanogenic bacteria; ethanol-type fermentation was the optimal acidogenci-type fermentation for the two-phase anaerobic process; the conversion of acetic acid was rather high, but the others organic acids will be convert to acetic acid make it the rate-limiting step for anaerobic degradation.

Acetic Acid↗
PubMed1995

Substrate specificity of nine NAD(+)-dependent alcohol dehydrogenases in Aspergillus nidulans.

In Aspergillus nidulans three alcohol dehydrogenases (ADHs) have been described. ADHI is induced by ethanol and is the physiological enzyme of ethanol utilization, ADHII has not been attributed a function but is repressed by ethanol. The ALCR regulatory protein acts positively to induce ADHI, and negatively in its control of ADHII. ADHIII is specifically induced by anaerobic stress. We have characterized the substrate specificity of these three enzymes by looking at their staining profile on polyacrylamide gels with a range of alcohols. In addition to these enzymes we have observed six other NAD(+)-dependent ADHs, two of which, propan-2-ol dehydrogenase and pentan-2-ol dehydrogenase, share similar control with ADHII. The inducibility of these enzymes with some alcohols has also been investigated. The profile of ADHs with NADP+ as an electron acceptor is also reported.

Alcohol Dehydrogenase↗
PubMed1989

Nutrient reabsorption of intestine in vitro: effects of ethanol and caffeine.

We studied the effect of ethanol and caffeine on the intestinal reabsorption (jejunum from SD rats) of glucose (Glu) and amino acids. Since most of the studies on the effect of ethanol utilized high concentration, we first characterized the effect of 8% (approximately 1.4 M) ethanol on the activity of Na(+)-coupled nutrient transport. Consistent with previous reports, ethanol (greater than 1 M) was found to inhibit the uptake rates of glucose and its non-metabolizable analogue 3-O-methyl-glucose (3-OMG) by 30%, while leucine (Leu) uptake was inhibited by 60%. Phloridzin, a specific inhibitor for Na(+)-coupled sugar transport, at 1 mM concentration could inhibit Glu and 3-OMG uptake by more than 60% without affecting Leu uptake. We then compared the effects of various concentrations of ethanol on about 20 intestinal segments taken from the same animal. We consistently observed transport inhibition at high concentration of ethanol but at low concentrations (up to 200 mM), there was no consistent effect, while phloridzin or low-Na media (86% of Na replaced by choline) significantly reduced the rate of nutrient uptake in the same experiment. Thus, it appeared that low concentrations of ethanol had no significant effect on Na(+)-coupled nutrient uptake. We also determined the effect of caffeine on intestinal 3-OMG uptake. At concentration of 0.05 mM, caffeine inhibited 3-OMG uptake by about 15% (p less than 0.05). The level of inhibition was not significantly different at 0.5 mM, but a slightly higher level of inhibition (20%) was reached at 5 mM. The action of caffeine could be mimicked by dibutyryl cAMP (1 mM).

3-O-Methylglucose↗
PubMed2006

Dihydroxyacetone detoxification in Saccharomyces cerevisiae involves formaldehyde dissimilation.

To investigate Saccharomyces cerevisiae physiology during growth on the conditionally toxic triose dihydroxyacetone (DHA), protein expression was studied in strains overexpressing either of the two dihydroxyacetone kinase isogenes, DAK1 or DAK2, that grow well utilizing DHA as a carbon and energy source. DHA metabolism was found mostly similar to ethanol utilization, involving a strong component of glucose derepression, but also involved DHA-specific regulatory changes. A specific and strong (10- to 30-fold induction of formaldehyde dehydrogenase, Fdhlp, indicated activation of the formaldehyde dissimilation pathway in DHA medium. The importance of this pathway was further supported by impaired adaptation to DHA growth and DHA survival in a glutathione-dependent formaldehyde dehydrogenase (SFA1) deletion mutant. Glutathione synthase (GSH1) deletion led to decreased DHA survival in agreement with the glutathione cofactor requirement for the SFA1-encoded activity. DHA toxicity did, however, not solely appear related to formaldehyde accumulation, because SFA1 overexpression only enhanced formaldehyde but not DHA tolerance. In further agreement with a low DHA-to-formaldehyde flux, GSH supplements in the low microM range also fully suppressed the DHA sensitivity of a gsh1Delta strain. Under growth reduction on high (100 mM) DHA medium we report increased levels of advanced glycation end-product (AGE) formation on total protein. Under these high-DHA conditions expression of several stress-related proteins, e.g. a heat-shock protein (Hsp104p) and the oxidative stress indicator, alkyl hydroperoxide reductase (Ahp1p) was also found induced. However, hallmark determinants of oxidative stress tolerance (e.g. YAP1, SKN7, HYR1/GPX3 and SOD2) were redundant for DHA tolerance, thus indicating mechanisms of DHA toxicity largely independent of central oxidative stress defence mechanisms. We conclude that mechanisms for DHA growth and detoxification appear complex and that the evolutionary strive to minimize detrimental effects of this intracellular metabolite links to both formaldehyde and glutathione metabolism.

Aldehyde Oxidoreductases↗
PubMed1999

Conditioning to ethanol in the fruit fly-a study using an inhibitor of ADH.

To identify processes involved in the choice of ethanol by adult Drosophila, flies homozygous Adh(F), reared in the absence of alcohol were placed in contact with: a) an ethanol-free medium, b) a medium containing ethanol, c) a medium supplemented with 4-methylpyrazole (4-MP, an inhibitor of the ADH pathway), d) a medium containing ethanol and 4-MP. The choice of ethanol over a medium without ethanol was evaluated by measuring the duration of extension of the proboscis of the flies in each of the media. A slight preference for the ethanol-supplemented medium was observed in the naive flies, which was enhanced by previous exposure to ethanol. Exposure to ethanol and 4-MP, however, led to an avoidance of ethanol. There was a reduction in ADH activity on treatment of the flies with 4-MP, and signs of malaise (reduced locomotor activity, loss of balance) were observed in the flies who ingested both ethanol and inhibitor. We concluded that the preference for ethanol stems from an associative learning related to ethanol utilization. Inhibition of enzymes of ADH pathway led to a conditioned aversion due to disturbance of ethanol metabolism giving rise to malaise.

Journal Article↗
PubMed1996

[The dynamics of 14C-ethanol and 14C-acetaldehyde distribution in rat testes].

Changes in radioactivity were studied during one day in common proteins, karyoplasm and chromatin of testis tissue and in the blood serum of rats after administration of (14C)ethanol and (14C)acetaldehyde. In a series of experiments the acetaldehyde involvement dynamics was determined on the background of disulphiram action. It has been found that the rate of elimination of indicator doses of ethanol and acetaldehyde from the blood varies within a day. In the interval (2-4 h) the ethanol utilization rate is higher than that of acetaldehyde. It is, probably, caused by the activity of ethanol transformation enzymes, intensive ethanol oxidation and inflow of the transformation products to the tissues. Karyoplasm had the highest level of radioactivity among the investigated testis structures. During the day the acetaldehyde accumulation rate per a unit of time was several times lower in chromatin, than in karyoplasm. These results permit supposing that the testis karyoplasm structures possess the mechanisms which inhibit acetaldehyde penetration into chromatin of the male generative cells.

Acetaldehyde↗
PubMedDate not supplied

DTI-015 produces cures in T9 gliosarcoma.

DTI-015 (BCNU in 100% ethanol) utilizes solvent-facilitated perfusion for the intratumoral treatment of gliomas. The water-miscible organic solvent vehicle, ethanol, facilitates a rapid and thorough saturation of the'tumor with the dissolved anticancer agent, BCNU. Rats bearing established intracranial T9 gliosarcoma tumors received no treatment (group 1), a single intratumoral injection of ethanol vehicle (group 2) or DTI-015 (5 mg/kg BCNU) (group 3), or a single intratumoral injection of DTI-015 followed by systemic BCNU (group 4). Ethanol alone (n=13) had no effect on survival; MST=17 days compared to 18 days for untreated controls (n=35). DTI-015 (n=45) produced an ILS of 417% (MST=93) and 472% (MST=103) when combined with systemic BCNU (n=14). Overall, 24 of 59 rats receiving DTI-015 were judged to be cured, with 20 living a normal life span of 600 to 700 days, and 4 rats sacrificed healthy at 121, 135, 307, and 384 days post DTI-015 with no evidence of viable T9 tumor. Histology demonstrated that DTI-015 totally eradicated the T9 tumors in animals living a normal life span. The results demonstrate that a single injection of DTI-015 produces a 40% cure rate in rats bearing established intracranial T9 tumors.

Animals↗
PubMed2001

Ethanol catabolism in Aspergillus nidulans: a model system for studying gene regulation.

This article reviews our knowledge of the ethanol utilization pathway (alc system) in the hyphal fungus Aspergillus nidulans. We discuss the progress made over the past decade in elucidating the two regulatory circuits controlling ethanol catabolism at the level of transcription, specific induction, and carbon catabolite repression, and show how their interplay modulates the utilization of nutrient carbon sources. The mechanisms featuring in this regulation are presented and their modes of action are discussed: First, AlcR, the transcriptional activator, which demonstrates quite remarkable structural features and an original mode of action; second, the physiological inducer acetaldehyde, whose intracellular accumulation induces the alc genes and thereby a catabolic flux while avoiding intoxification; third, CreA, the transcriptional repressor mediating carbon catabolite repression in A. nidulans, which acts in different ways on the various alc genes; Fourth, the promoters of the structural genes for alcohol dehydrogenase (alcA) and aldehyde dehydrogenase (aldA) and the regulatory alcR gene, which exhibit exceptional strength compared to other genes of the respective classes. alc gene expression depends on the number and localization of regulatory cis-acting elements and on the particular interaction between the two regulator proteins, AlcR and CreA, binding to them. All these characteristics make the ethanol regulon a suitable system for induced expression of heterologous protein in filamentous fungi.

Alcohol Dehydrogenase↗
PubMed1997

Impairment of peroxisome degradation in Pichia methanolica mutants defective in acetyl-CoA synthetase or isocitrate lyase.

Single recessive mutations of the methylotrophic yeast Pichia methanolica acs1, acs2, acs3 and icl1 affecting acetyl-CoA synthetase and isocitrate lyase, and growth on ethanol as sole carbon and energy source, caused a defect in autophagic peroxisome degradation during exposure of methanol-grown cells to ethanol. As a control, a mutation in mdd1, which resulted in a defect of the 'malic' enzyme and also prevented ethanol utilization, did not prevent peroxisome degradation. Peroxisome degradation in glucose medium was unimpaired in all strains tested. Addition of ethanol to methanol-grown cells of acs1, acs2, acs3 and icl1 mutants led to an increase in average vacuole size. Thickening of peroxisomal membranes and tight contacts between groups of peroxisomes and vacuoles were rarely observed. These processes proceeded much more slowly than in wild-type or mdd1 mutant cells incubated under similar conditions. No peroxisomal remnants were observed inside vacuoles in the cells of acs1, acs2, acs3 and icl1 mutants after prolonged cultivation in ethanol medium. We hypothesize that the acs and icl mutants are defective in synthesis of the true effector--presumably glyoxylate--of peroxisome degradation in ethanol medium. Lack of the effector suspends peroxisome degradation at an early stage, namely signal transduction or peroxisome/vacuole recognition. Finally, these defects in peroxisome degradation resulted in mutant cells retaining high levels of alcohol oxidase which further led to increased levels of acetaldehyde accumulation upon incubation of mutant cells with ethanol.

Acetaldehyde↗
PubMed2003

Formation of DNA adducts and tumor growth delay following intratumoral administration of DTI-015.

Intratumoral (IT) administration of DTI-015 (BCNU in 100% ethanol) utilizes solvent facilitated perfusion for the treatment of tumors. RIF-1 tumors were treated by IT injection of either ethanol alone or 0.05-1.0 mg of DTI-015 or by i.v. injection of 0.5 mg of BCNU. Treatment with ethanol alone or i.v. injection of 0.5 mg of BCNU did not produce a significant growth delay. In contrast, IT administration of DTI-015 produced a significant growth delay at each of the treatment doses (p < 0.05 to p < 0.001). We have quantified the levels of N7-(2-hydroxyethyl) guanine (N7-HOEtG) in RIF-1 tumors 24h following either IT treatment with 0.5 mg DTI-015 or i.p. administration of 0.5 mg BCNU. Levels of N7-HOEtG (micromol/mol DNA) were < or = 0.08 for both untreated controls and following i.p. treatment with BCNU and 13.1 +/- 5.6 following IT administration of DTI-015. The levels of N7-HOEtG detected in RIF-1 tumors following IT administration of DTI-015 were 164-fold higher than the level(s) of N7-HOEtG in the i.p. BCNU treated tumor samples. These studies demonstrate that IT administration of DTI-015 produces high levels of DNA adducts in the tumor which correspond to a significant increase in tumor growth delay compared to the same dose of BCNU administered systemically.

Animals↗