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PubMedDate not supplied

[Role of ethanol tolerance in determining a hereditary disposition to alcoholism].

Genetic-correlative analysis of the tolerance level, amount of alcohol consumed (ml/kg for 1 year) as well as predisposition to the development of alcoholism permitted an assumption on existence of two different genetic factors one of which determined the tolerance level and the other one-predisposition to disease.

Adult↗
PubMedDate not supplied

Gene array-based identification of changes that contribute to ethanol tolerance in ethanologenic Escherichia coli: comparison of KO11 (parent) to LY01 (resistant mutant).

Escherichia coli KO11 (parent) and LY01 (mutant) have been engineered for the production of ethanol. Gene arrays were used to identify expression changes that occurred in the mutant, LY01, during directed evolution to improve ethanol tolerance (defined as extent of growth in the presence of added ethanol). Expression levels for 205 (5%) of the ORFs were found to differ significantly (p < 0.10) between KO11 and LY01 under each of six different growth conditions (p < 0.000001). Statistical evaluation of differentially expressed genes according to various classification schemes identified physiological areas of importance. A large fraction of differentially expressed ORFs were globally regulated, leading to the discovery of a nonfunctional fnr gene in strain LY01. In agreement with a putative role for FNR in alcohol tolerance, increasing the copy number of fnr(+) in KO11(pGS196) decreased ethanol tolerance but had no effect on growth in the absence of ethanol. Other differences in gene expression provided additional clues that permitted experimentation. Tolerance appears to involve increased metabolism of glycine (higher expression of gcv genes) and increased production of betaine (higher expression of betIBA and betT encoding betaine synthesis from choline and choline uptake, respectively). Addition of glycine (10 mM) increased ethanol tolerance in KO11 but had no effect in the absence of ethanol. Addition of betaine (10 mM) increased ethanol tolerance by over 2-fold in both LY01 and KO11 but had no effect on growth in the absence of ethanol. Both glycine and betaine can serve as protective osmolytes, and this may be the basis of their beneficial action. In addition, the marAB genes encoding multiple antibiotic resistance proteins were expressed at higher levels in LY01 as compared to KO11. Interestingly, overexpression of marAB in KO11 made this strain more ethanol-sensitive. Overexpression of marAB in LY01 had no effect on ethanol tolerance. Increased expression of genes encoding serine uptake (sdaC) and serine deamination (sdaB) also appear beneficial for LY01. Addition of serine increased the growth of LY01 in the presence and absence of ethanol but had no effect on KO11. Changes in the expression of several genes concerned with the synthesis of the cell envelope components were also noted, which may contribute to increased ethanol tolerance.

Directed Molecular Evolution↗
PubMed2006

Ethanol tolerance caused by slowpoke induction in Drosophila.

BACKGROUND: The large-conductance calcium-activated potassium channel encoded by the slowpoke gene has recently been implicated in the ethanol response. Caenorhabditis elegans carrying mutations in this gene have altered ethanol sensitivity and Drosophila mutant for this gene are unable to acquire rapid tolerance to ethanol or anesthetics. In Drosophila, induction of slowpoke expression has been linked to anesthetic resistance. METHODS: We used Drosophila as a model system to examine the relationship between slowpoke expression and ethanol tolerance. Real-time PCR and a reporter transgene were used to measure slowpoke induction after ethanol sedation. An inducible slowpoke transgene was used to manipulate slowpoke levels in the absence of ethanol sedation. RESULTS: Ethanol sedation increased transcription from the slowpoke neural promoters but not from the slowpoke muscle/tracheal cell promoters. This neural-specific change was concomitant with the appearance of ethanol tolerance, leading us to suspect linkage between the two. Moreover, induction of slowpoke expression from a transgene produced a phenotype that mimics ethanol tolerance. CONCLUSIONS: In Drosophila, ethanol sedation induces slowpoke expression in the nervous system and results in ethanol tolerance. The induction of slowpoke expression alone is sufficient to produce a phenotype that is indistinguishable from true ethanol tolerance. Therefore, the regulation of the slowpoke BK-type channel gene must play an integral role in the Drosophila ethanol response.

Animals↗
PubMed1992

Effect of growth rate on ethanol tolerance of Saccharomyces cerevisiae.

delta 5,7-Sterol-accumulating Saccharomyces cerevisiae cells growing in chemostat at a specific growth rate of 0.075/h exhibited higher ethanol tolerance measured as ethanol-induced death and anaerobic growth inhibition than the cells growing at 0.2/h, the difference being dependent on the carbon-to-nitrogen molar proportion in the medium. The observed difference in sensitivity to ethanol of anaerobic growth between the slowly and rapidly-growing cells was completely reversed as a result of a block in sterol synthesis causing a negligible synthesis of delta 5,7-sterols. Two physiological parameters, budding frequency and membrane composition, evidently affected ethanol tolerance. Differences between the delta 5,7-sterol-synthesizing and deficient strains documented a profound effect of the quality of the sterol present on the physiological state of the cell.

Anaerobiosis↗
PubMed2006

Isolation and characterization of two novel ethanol-tolerant facultative-anaerobic thermophilic bacteria strains from waste compost.

In a search for potential ethanologens, waste compost was screened for ethanol-tolerant thermophilic microorganisms. Two thermophilic bacterial strains, M5EXG and M10EXG, with tolerance of 5 and 10% (v/v) ethanol, respectively, were isolated. Both isolates are facultative anaerobic, non-spore forming, non-motile, catalase-positive, oxidase-negative, Gram-negative rods that are capable of utilizing a range of carbon sources including arabinose, galactose, mannose, glucose and xylose and produce low amounts of ethanol, acetate and lactate. Growth of both isolates was observed in fully defined minimal media within the temperature range 50-80 degrees C and pH 6.0-8.0. Phylogenetic analysis of the 16S rDNA sequences revealed that both isolates clustered with members of subgroup 5 of the genus Bacillus. G+C contents and DNA-DNA relatedness of M5EXG and M10EXG revealed that they are strains belonging to Geobacillus thermoglucosidasius. However, physiological and biochemical differences were evident when isolates M5EXG and M10EXG were compared with G. thermoglucosidasius type strain (DSM 2542(T)). The new thermophilic, ethanol-tolerant strains of G. thermoglucosidasius may be candidates for ethanol production at elevated temperatures.

Bacillaceae↗
PubMed1987

Endothelium-dependent transfer of ethanol tolerance in the aorta.

Recent studies have suggested that the endothelium-dependent tolerance to the direct vasoconstrictor effect of ethanol in the rat aorta is mediated by endothelium-derived relaxing factor (EDRF). This hypothesis was tested directly by employing a sandwich technique which has been used to demonstrate the release and action of EDRF. These experiments measured the ethanol-induced contraction of a spirally-cut aortic strip without endothelium obtained from an ethanol naive control rat. The response of the spiral strip was measured before and after it was sandwiched with a longitudinally-cut aortic strip with or without endothelium obtained from either control or ethanol tolerant rats. There was no significant difference in the ethanol-induced contraction of the spiral strip after beginning sandwiched with a longitudinal strip with or without endothelium obtained from a control rat or with a longitudinal strip without endothelium from a tolerant rat. In contrast, when a longitudinal strip with endothelium from a tolerant rat was sandwiched with the spiral strip the ethanol-induced contraction was significantly reduced. This effect was inhibited by methylene blue but not by indomethacin. Further, the magnitude of the carbachol-induced relaxation of the sandwiched preparation was significantly greater when the longitudinal strip with endothelium was obtained from a tolerant rat than from control rat. These data demonstrate the involvement of EDRF in the endothelium-dependent tolerance to ethanol in the rat aorta.

Animals↗
PubMed1989

Alcohol dehydrogenase and ethanol tolerance at the cellular level in Drosophila melanogaster.

Exposure of early third instar larvae of Drosophila melanogaster to a nonlethal dose of ethanol was detrimental to larvae lacking alcohol dehydrogenase (ADH) but beneficial to wild-type larvae in terms of surviving a later ethanol tolerance test, indicating that one of the important functions of the ADH system is to supply derivatives of ethanol to larvae that in turn promote ethanol tolerance. High intracellular concentrations of ethanol in ADH-deficient (Adhn2) larvae fed ethanol were accompanied by a decrease in the cell membrane infoldings of fat body cells, suggesting that the capacities to absorb and release molecules were reduced. Marked effects of ethanol on the endoplasmic reticulum and mitochondria of ADH-deficient larvae were also evident. The absence of similar changes in wild-type larvae that were fed moderate levels of ethanol showed that the ADH system kept the intracellular level of ethanol at a concentration low enough to avoid cell damage. A cytometric analysis of electron micrographs showed that there were ethanol-induced reductions in glycogen, lipid, and protein stores in the fat body cells of ADH-deficient larvae fed 1.25% ethanol (v/v) compared with null larvae fed an ethanol-free diet. This finding implied that the capacities to synthesize or store these compounds may be limited by high intracellular concentrations of ethanol. The cytometric analysis also revealed that the consumption of diets containing 2.5% and 4.5% ethanol by Canton-S wild-type larvae for 3 days after 4 days of feeding on an ethanol-free diet resulted in decreases in glycogen and protein deposits in fat body cells, but increased the amount of lipid deposits compared to larvae fed an ethanol-free diet. This observation, coupled with the greater weight of wild-type adults that were fed a growth-limiting concentration of ethanol compared with control adults, suggested that a metabolic defense mechanism in larvae is to convert toxic ethanol to nontoxic storage products. Dietary ethanol alone and in combination with isopropanol stimulated an increase in the size of the NAD-pool in larvae, a condition that may favor the activity of ADH. A low dietary level of isopropanol (1%) completely blocked glycogen deposition in wild-type larvae, whereas ethanol did not. Thus ethanol and isopropanol exert some different toxic effects on larval fat bodies.

Alcohol Dehydrogenase↗
PubMed1996

Gangliosides reduce the development of ethanol dependence without affecting ethanol tolerance.

Mice given an ethanol-containing liquid diet, as their sole source of nutrients and fluid, rapidly developed functional tolerance to and physical dependence on ethanol. The presence of physical dependence was demonstrated by measured signs of central nervous system hyperexcitability upon withdrawal of ethanol. The withdrawal hyperexcitability, which included tremors, handling-induced seizures and spontaneous clonic/tonic seizures, was more pronounced when mice consumed the ethanol-containing diet for 7 days, compared with 5 days. Daily treatment of the animals with either a ganglioside mixture (extracted bovine brain gangliosides, 250 or 500 mg/kg i.p.) or ganglioside GM1 (100 mg/kg i.p.) for the terminal two-thirds of the ethanol administration period resulted in a significant reduction in the ethanol withdrawal signs. On the other hand, tolerance to the hypnotic action of ethanol, tested 30 hr after withdrawal of ethanol, was unaffected by ganglioside treatment. Ganglioside GM1 given i.c.v. at a daily dose of 10 micrograms during the ethanol ingestion period was as effective as 100 mg/kg GM1 given i.p. in reducing signs of ethanol withdrawal. The daily administration of gangliosides during the feeding of the ethanol diet did not alter the animals' ethanol consumption, intoxication or blood ethanol levels at the time of ethanol withdrawal. A single dose of GM1 given either i.p. or i.c.v. 16 hr before withdrawal produced no effect on the measured ethanol withdrawal signs. Our prior work and the work of others has demonstrated a relationship between up-regulation of N-methyl-D-aspartate receptor numbers in brain and the manifestation of ethanol withdrawal signs. Daily administration of GM1, during the last 5 days of a 7-day period of ethanol ingestion, prevented the up-regulation of N-methyl-D-aspartate receptors in the hippocampus and reduced the ethanol withdrawal signs. Our data demonstrate that the daily administration of gangliosides during the period of ethanol consumption may prevent the development of ethanol physical dependence, while leaving ethanol tolerance intact.

Animals↗