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Results for “ethanol tolerance”

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At least 19 recordsLinked to original sources
PubMed1979

Selection for ethanol tolerance in two populations of Drosophila melanogaster segregating alcohol dehydrogenase allozymes.

Selection for ethanol tolerance was equally successful in two populations of D. melanogaster in both of which the frequency of AdhF was 0.5 at the start of the experiment. Increased tolerance to ethanol was not invariably associated with increased frequencies of AdhF. In one population alcohol dehydrogenase (ADH) activity was significantly higher in three of the four selected sublines compared with their controls but there was no difference in activity between the selected and control sublines in the second population. The level of ADH activity in the control and selected lines was significantly correlated with the frequency of AdhF, but not with ethanol tolerance. These results show that adaptation to environmental alcohols in populations of D. melanogaster can be independent of the ADH system.

Alcohol Oxidoreductases↗
PubMedDate not supplied

Genetics and ethanol tolerance.

This paper reviews some of the research on genetic bases of individual differences in ethanol tolerance of mice conducted at the Institute for Behavioral Genetics and at its predecessor laboratory at the University of California, Berkeley. Tolerance is, of course, a complex concept. Theoretical distinctions are made between tachyphylaxis and more slowly acquired tolerance and between dispositional and tissue tolerance. Pragmatically, a variety of measures (such as locomotor activity, sleep time, hypothermia) can be used to define these processes, and the different indices may yield quite different results even when they presumably indicate the same process. It is clear that an understanding of genetic influence in "ethanol tolerance" will require wide sampling of this complex domain. The work described here represents only a beginning, but it may illustrate the general approaches that are available for addressing the issue.

Alcohol Drinking↗
PubMed1979

Effect of modification of brain serotonin (5-HT) on ethanol tolerance.

The effects of 5,7-dihydroxytryptamine and L-tryptophan treatment on ethanol tolerance in the rat, as measured by the moving-belt test of motor impairment and by hypothermia, were examined in separate studies. A 2 x 2 design was used for all experiments. 5,7-Dihydroxytryptamine (200 microgram in 20 microliter CSF) or vehicle alone was administered once into both lateral ventricles of the rat. Desmethylimipramine was administered intraperitoneally prior to an intraventricular injection of 5,7-dihydroxytryptamine to prevent the destruction of norepinephrine. L-Tryptophan (75 mg/kg p.o. twice daily) or water was administered chronically. Ethanol (4--5 g/kg p.o.) or sucrose was given daily, and the development of tolerance was monitored at 5--7-day intervals. Chronic ethanol treatment produced tolerance to both the motor impairment and hypothermia effects of ethanol. 5,7-Dihydroxytryptamine and L-tryptophan treatment did not alter either the motor impairment or hypothermia produced by the initial dose of ethanol. 5,7-Dihydroxytryptamine produced a 75% depletion of brain 5-HT and slowed the development of tolerance to ethanol in both measurements. In contrast, elevation of 5-HT by L-tryptophan (39% increase by a single dose) facilitated the development of tolerance to ethanol, as seen in both measures. These findings support our hypothesis that brain 5-HT has a modulating role in the development of tolerance to ethanol.

5,7-Dihydroxytryptamine↗
PubMed2025

Adaptive laboratory evolution of Saccharomyces cerevisiae CEN.PK 113-7D to enhance ethanol tolerance.

Saccharomyces cerevisiae is a widely used yeast for industrial production of ethanol. However, elevated ethanol, temperature, and osmotic stress adversely affect fermentation efficiency. In this study, adaptive laboratory evolution for S. cerevisiae CEN.PK 113-7D on higher concentrations of ethanol was performed. After 144 days, the maximum specific growth rate (&#xb5;max) increased from 0.0240 to 0.1150 h-1 for the strain evolved on 9% v/v ethanol, and from 0.0002 to 0.0530 h-1 for the strain evolved on 11% v/v ethanol, and the specific glucose uptake rate increased by 30%. The strain evolved on 11% ethanol produced 94.5&#xa0;g/L ethanol in a fermentation as compared to 78.5&#xa0;g/L production by a non-evolved strain. By whole-genome sequencing of the evolved clones, we identified multiple coding mutations in genes involved in processes such as stress response, cell growth regulation, pentose phosphate pathway, lipid synthesis, and redox balance. The selected mutations in RKI1, CYC2, ANR2, RGA2, RGA1, LPX1, and LRE1 genes were validated by introducing them in the nonevolved yeast, showing 1.7-5-fold growth improvement at 9% ethanol (P&#xa0;<&#xa0;0.05). Notably, RGA2, RGA1 and LPX 1 carried an identical missense mutation across three independent clones. The RKI1I208V mutant showed the highest ethanol tolerance, while CYC2N342A achieved the highest ethanol production.

Ethanol↗
PubMedDate not supplied

Cyclic nucleotides and ethanol tolerance and dependence.

Acute ethanol administration decreases cyclic AMP levels in brains of some animal strains. The ethanol-induced decrease of cyclic GMP levels cannot be blocked by intraventricular infusion of calcium but it can be prevented by pretreatment with pyrazole. Although cyclic AMP levels in the cerebral cortex change reciprocally after acute ethanol administration and during withdrawal, the increase observed during withdrawal is probably secondary to some withdrawal processes. Ethanol decreases cerebellar GABA levels only in rats which are stressed prior to sacrifice. Chronic intraventricular infusion of calcium increased the intensity of an acoustic startle response during ethanol withdrawal while EGTA infusion delayed the development of tolerance to the hypothermic effect of ethanol. The ratio of cyclic GMP to GABA levels is postulated to be important for expression of the withdrawal syndrome.

Animals↗
PubMedDate not supplied

Adaptive changes in membrane lipid composition and fluidity as the basis for ethanol tolerance.

This paper is intended as a brief commentary on the evidence for adaptation to ethanol at the level of the cell membrane with more detailed consideration of the possible mechanisms for such adaptation. Methodological and conceptual problems are raised and the current views of ethanol tolerance at the membrane level are criticised. The paper includes an abstract of work carried out by the author's group on changes in membrane phospholipid composition of mice during exposure to ethanol by inhalation.

Animals↗
PubMedDate not supplied

Peptide--neurotransmitter interactions influencing ethanol tolerance.

Chronic exposure of mice to ethanol leads to the development of functional tolerance to the hypothermic and sedative effects of this drug. Treatment of the animals with the mammalian antidiuretic hormone, arginine vasopressin, results in a prolonged duration of such tolerance, in comparison to animals exposed to ethanol but not to the hormone. Another neurohypophyseal hormone, oxytocin, at an equimolar dose, is ineffective in maintaining tolerance. The centrally mediated effects of arginine vasopressin on memory processes may be related to the hormone-induced prolongation of ethanol tolerance.

Animals↗
PubMedDate not supplied

Mechanisms of ethanol tolerance at a cholinergic nerve terminal.

In vitro rat phrenic nerve-diaphragm preparations illustrated a concentration-dependent increase in the spontaneous release (miniature end-plate potentials, MEPPs) of acetylcholine following acute administration of ethanol. In phrenic nerve terminals from rats subjected to long-term ethanol treatmet, ethanol in vitro was significantly less effective in increasing the frequency of MEPPs. The capacity of ethanol administration to change membrane viscosity and alter sequestration of intracellular Ca2+ is discussed as a possible explanation for the observed effects.

Acetylcholine↗
PubMed1978

Plasma-membrane lipid composition and ethanol tolerance in Saccharomyces cerevisiae.

Populations of cells suspended anaerobically in buffered (pH 4.5) M ethanol remained viable to a greater extent when their plasma membranes were enriched in linoleyl rather than oleyl residues irrespective of the nature of the sterol enrichment. However, populations with membranes enriched in ergosterol or stigmasterol and linoleyl residues were more resistant to ethanol than populations enriched in campesterol or cholesterol and linoleyl residues. Populations enriched in ergosterol and cetoleic acid lost viability at about the same rate as those enriched in oleyl residues, while populations grown in the presence of this sterol and palmitoleic acid were more resistant to ethanol. Suspending cells in buffered ethanol for up to 24 h did not lower the ethanol concentration.

Anaerobiosis↗
PubMed1975

Electroencephalographic signs of ethanol tolerance and physical dependence in the cat.

Spontaneous electrical activity was recorded from three cortical and five subcortical sites, via permanently implanted electrodes, in five conscious, freely-moving adult cats. Initial observations were made during and after an intravenous infusion of ethanol, 1 g/kg. The animals then received ethanol by gastric intubation, in doses of 1.5 g/kg every 8, 12 or 24 h, for a period of 5 weeks. Electrical and behavioral observations were repeated on the day following the last gavage, before and during another intravenous infusion of ethanol 1 g/kg. All animals showed EEG changes which are interpreted as signs of tolerance to and dependence on alcohol. EEG changes appeared up to a day earlier than gross behavioral signs of alcohol withdrawal.

Action Potentials↗
PubMed1978

Effect of tolerance to morphine, ethanol and barbiturate on amphetamine circling in rats with a striatal dopamine lesion.

The (+)-amphetamine circling rate of rats with unilateral 6-OHDA lesions in the striatum was recorded. Morphine tablets were implanted subcutaneously for chronic treatment. In the morphine-dependent animal the circling rate to amphetamine given 4 days after morphine was first implanted was depressed but after withdrawal with naloxone a day later the rate increased, returning to normal after 21 days. Barbiturate physical dependence was induced by adding increasing amounts of barbitone to the drinking water of lesioned rats over four weeks after which the amphetamine circling response was depressed and remained so after the barbituate was withdrawn. Ethanol tolerance was induced by adding ethanol to the drinking water of lesioned rats for four weeks. Neither the induction of tolerance over this period nor ethanol withdrawal had any effect on the circling response to amphetamine. The change in the response of striatal dopamine neurons to amphetamine that occurs after chronic morphine treatment, cannot be produced by chronic treatment with either barbitone or ethanol. The neurochemical bases of barbiturate and ethanol tolerance are different from morphine tolerance.

Animals↗
PubMed1978

Effect of p-chlorophenylalnine on the loss and maintenance of tolerance to ethanol.

Rats were rendered tolerant to the motor-impairing effects of ethanol by daily oral administration. Subsequently, ethanol was withdrawn and the effect of p-chlorophenylalanine (p-CPA) on tolerance loss was examined. In two separate studies it was demonstrated that p-CPA, in a dosage regimen that produces extensive depletion of brain serotonin (5-HT), accelerated tolerance loss. These experiments suggest that at least part of p-CPA's inhibitory effect on net tolerance development to ethanol can be accounted for by its accelerating effect on tolerance loss; however, an inhibitory effect on tolerance acquisition cannot be excluded. On the other hand, once tolerance was established, p-CPA did not affect the maintenance of tolerance to ethanol.

Animals↗