Disease relevance of Etohc1

• These data continue to suggest that, as a consequence of enhanced lipid peroxidation resulting from chronic ethanol consumption, increased 4-HNE levels could compromise cellular elimination of ethanol-derived acetaldehyde and thus function in the potentiation of alcoholic liver fibrosis [1].
• Taken together, these findings suggest that ethanol consumption (as well as exposure to other 'spindle-acting' agents) at the time of conception may be the cause of certain types of chromosomal defects commonly observed in human spontaneous abortions [2].
• Chronic ethanol consumption marginally reduced the levels of the antibody to hepatitis B surface proteins (anti-HBs) generated by the DNA-based immunization approach [3].
• In conclusion, these results suggest that HCV core protein cooperates with ethanol for the activation of some MAPK pathways, and leads to the modulation of several genes, contributing to the pathogenesis of liver disease of HCV-infected patients with high ethanol consumption [4].
• Inhibitory effects of chronic ethanol consumption on cellular immune responses to hepatitis C virus core protein are reversed by genetic immunizations augmented with cytokine-expressing plasmids [5].

Psychiatry related information on Etohc1

• What is more, we investigated voluntary alcohol consumption in Per2 ( Brdm1 ) mice with the results suggesting a relationship between this circadian clock gene and ethanol consumption [6].
• In terms of alcohol drinking behavior, compared to wild-types, GluR1-/- mice differed neither in the acquisition of voluntary ethanol consumption nor in stress-induced ethanol drinking, nor in the expression of an alcohol deprivation effect (ADE) which is used as a model of relapse-like drinking behavior [7].
• RATIONALE: The development of mouse models of ethanol consumption and ethanol-seeking behavior is of particular importance in understanding the underlying mechanisms of drug abuse because these models can enable an analysis of an effect of specific genotype on drug-seeking behavior and the interaction of potential therapeutics with genotype [8].
• A retinoic acid receptor antagonist suppresses brain retinoic acid receptor overexpression and reverses a working memory deficit induced by chronic ethanol consumption in mice [9].
• In addition, injection-free animals were tested for ethanol consumption on day 16 after an overnight water deprivation period [10].

High impact information on Etohc1

• Here we report that mice lacking Eps8, a regulator of actin dynamics, are resistant to some acute intoxicating effects of ethanol and show increased ethanol consumption [11].
• Treatment with an A(1) receptor agonist decreases EPSC amplitude and reduces ethanol consumption in ENT1-null mice [12].
• Ethanol consumption increased levels of protein carbonyls and lipid peroxidation aldehydic products in the liver of Sod1(-/-) mice [13].
• In conclusion, a rather moderate ethanol consumption promoted oxidative stress in Sod1(-/-) mice, with increased formation of peroxynitrite, protein carbonyls, and lipid peroxidation and decreased mitochondrial GSH and MnSOD [13].
• A male-specific locus on proximal chromosome 8 (Ap8q) affected 3% ethanol preference, but not indexes of 10% ethanol consumption [14].

Chemical compound and disease context of Etohc1

• The effect of chronic ethanol consumption on acetaminophen (200, 400, and 600 mg/kg) toxicity was determined by maintaining mice for 10 days on diets consisting of chow and one of the following drinking solutions: 10% ethanol + 10% sucrose, 8% sucrose, or tap water [15].
• Therapeutic dietary modifications are recommended including reduction of ethanol consumption, avoidance of excess selenium, copper, and zinc, and dietary promotion of magnesium (Mg(2+)), which is an essential co-factor for this enzyme [16].
• The influence of ethanol consumption on cleft palate induction by methylmercury, cortisone, and retinyl acetate was investigated in Swiss white mice [17].

Biological context of Etohc1

• Genes on mouse chromosomes 2 and 9 determine variation in ethanol consumption [18].
• The lipid peroxidation end products malondialdehyde and protein carbonyl formation were significantly elevated in both livers and hearts after chronic ethanol consumption, with the cardiac lipid and protein damage being exaggerated by ADH transgene [19].
• Voluntary ethanol consumption by mice: genome-wide analysis of quantitative trait loci and their interactions in a C57BL/6ByJ x 129P3/J F2 intercross [14].
• The loci with significant and suggestive linkages accounted for 35-44% of the genetic variation in ethanol consumption phenotypes [14].
• Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice [20].

Anatomical context of Etohc1

• The effect of a hypoproteic diet and ethanol consumption on the yield of chromosomal damage detected in bone marrow cells of mice [21].
• Chronic ethanol consumption by mice results in activated splenic T cells [22].
• The present study examined effects of chronic ethanol consumption on fluidity of synaptic plasma membrane (SPM) exofacial and cytofacial leaflets using trinitrobenzenesulfonic acid (TNBS) labeling and differential polarized fluorometry of 1,6-diphenyl-1,3,5-hexatriene (DPH) [23].
• Association of protein kinase C with GABA(A) receptors containing alpha1 and alpha4 subunits in the cerebral cortex: selective effects of chronic ethanol consumption [24].
• The oxidation chemistry of salsolinol-1-carboxylic acid (1), an alkaloid endogenous to the central nervous system which is elevated as a result of ethanol consumption, has been studied by electrochemical approaches at pH 7.0 in aqueous solution [25].

Associations of Etohc1 with chemical compounds

• Ethanol consumption increased the frequency of chromosomal damage, but no differences in the effect of ethanol between mice fed with the normal diet and mice fed with the hypoproteic diet (16.33 and 16.80 dicentrics per 100 cells respectively) [21].
• After 6 months of ethanol consumption we have observed in mouse liver an increased expression of Tri-iodothyronine receptors (TR) while the expression of retinoic acid (RA) receptors (RAR) was unaffected [26].
• Data indicate that iron deficiency and/or chronic ethanol consumption induce adverse effects on maternal reproductive performance of CBA/J mice possibly via alteration of folate metabolism [27].
• After chronic ethanol consumption, microsomal ethanol-oxidizing system (MEOS) activity increases with an associated rise in microsomal cytochrome P-450, including a form different from that induced by phenobarbital and methylcholanthrene and which has a high affinity for ethanol, as shown in reconstituted systems [28].
• The mGluR5 antagonist 6-methyl-2-(phenylethynyl)pyridine decreases ethanol consumption via a protein kinase C epsilon-dependent mechanism [29].

Physical interactions of Etohc1

• Changes in neurotensin receptor binding in mice after chronic ethanol consumption [30].

Regulatory relationships of Etohc1

• Here we show that chronic ethanol consumption induces significant apoptosis in the liver of IL-6 (-/-) mice but not IL-6 (+/+) mice [31].
• BACKGROUND: Recent genetic and pharmacological evidence indicates that low neuropeptide Y (NPY) levels in brain regions involved with neurobiological responses to ethanol promote increased ethanol consumption [32].
• In this study we determined, first, whether acute tolerance to ethanol inhibition is mediated via NR2B-containing NMDARs in vivo and, second, whether the increase in acute sensitivity to ethanol in the Fyn-/- mice influences ethanol consumption or ethanol's conditioned rewarding effects [33].
• Ethanol consumption suppresses the IL2-induced proliferation of NK cells [34].
• Results from the present study indicate that the gene encoding the neuronal-specific gamma subtype of protein kinase C (PKCgamma) influences both ethanol consumption and behavioral impulsivity, a personality characteristic associated with Type II alcoholics, in a pleiotropic manner [35].

Other interactions of Etohc1

• The similarity in the response to ethanol consumption in animals fed either with the normal or the hypoproteic diet might have been provoked by a decrease of alcohol dehydrogenase (ADH) level in undernourished mice [21].
• Rodents have been extensively utilized to study ethanol's rewarding and aversive effects, and to demonstrate the existence of genetic influences on traits such as free-choice ethanol-consumption, ethanol-conditioned place preference and ethanol-conditioned taste aversion [18].
• Following prolonged ethanol consumption, an enhancement of both MEOS activity as well as the rates of ethanol metabolism occurs; the latter persisted despite inhibition of ADH by pyrazole and catalase by sodium axide, suggesting the involvement of MEOS in the adaptive increase [36].
• Compared to wild types, preference and consumption of ethanol were decreased in D1A2A receptor knockout mice, the reduction in ethanol consumption greater even than that seen in D1 receptor-deficient mice [37].
• However, the loss of NR2A does not alter other measures of acute ethanol intoxication or ethanol consumption, possibly implicating other NMDA subunits in these effects [38].

Analytical, diagnostic and therapeutic context of Etohc1

• The purpose of the current investigation was to verify or eliminate from further consideration putative QTLs for free-choice ethanol consumption originally identified in BXD Recombinant Inbred (RI) strains and other informative genetic crosses [18].
• We conclude that low but persistent ethanol consumption delays the onset and halts the progression of collagen-induced arthritis by interaction with innate immune responsiveness [39].
• Combined effects of moderate ethanol consumption and a low-protein diet during gestation on brain development in BALB/c mice [40].
• Long-term ethanol consumption at low to moderate levels exerts cardioprotective effects in the setting of ischemia and reperfusion (I/R) [41].
• BACKGROUND: Topiramate has recently been found to be more effective than placebo as an adjunct treatment for alcohol dependence, but it has not yet been investigated in animal models of ethanol consumption [42].

References