Disease relevance of Etohi1

• Mutants were less sensitive than wild-types on a test of ethanol-induced ataxia and, with repeated drug administration, tended to develop tolerance more slowly [1].
• Ethanol-induced chromosomal abnormalities at conception [2].
• Calcium, other divalent cations, and calcium antagonists were tested for their ability to alter ethanol-induced sleeping time, hypothermia, and behavioral intoxication in mice and rats [3].
• Differential contributions of c3, c5, and decay-accelerating factor to ethanol-induced Fatty liver in mice [4].
• Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity [5].

Psychiatry related information on Etohi1

• The presence or absence of an ethanol-induced increase in locomotor activity was not dependent on the sex or number of mice or rats tested [6].
• Although WSP and WSR mice do not differ in threshold for seizures elicited by electroconvulsive shock (ECS), WSR mice are more sensitive to ethanol-induced elevation of ECS seizure thresholds [7].
• These results suggest that ethanol-induced amnesia is related to BZP receptors and a dysfunction of the cholinergic neuronal system [8].
• Moreover, the ethanol-induced sleeping time was prolonged by approximately 60-100% (P < 0.01) in mice exposed to psychological stress for 30-120 min [9].
• Because differences among the LSXSS RI strains are large and highly reliable, they should be valuable animal models for testing more searching hypotheses about the etiology of individual differences in ethanol-induced anesthesia [10].

High impact information on Etohi1

• NPY-deficient mice are also less sensitive to the sedative/hypnotic effects of ethanol, as shown by more rapid recovery from ethanol-induced sleep, even though plasma ethanol concentrations do not differ significantly from those of controls [11].
• Moreover, weaver mutant mice, which have a missense mutation in the GIRK2 channel, showed a loss of ethanol-induced analgesia [12].
• Sensitivity to ethanol-induced locomotor impairment was also reduced in these mutant mice, although they showed a normal locomotor depressant response to the dopamine D1 antagonist SCH-23390 [13].
• In contrast to the protective effect of C3-/- against ethanol-induced steatosis, levels of both alanine aminotransferase and tumor necrosis factor alpha were increased in C3-/- mice after ethanol feeding [4].
• Early growth response-1 transcription factor is essential for ethanol-induced fatty liver injury in mice [14].

Chemical compound and disease context of Etohi1

• Several rodent studies have also suggested that intact 5-HT systems are important determinants of sensitivity and/or tolerance to ethanol-induced ataxia and hypothermia [1].
• Based on the hypothesis that drugs of abuse increase locomotor activity through mechanisms related to reinforcement, i.e. the mesolimbic dopamine (DA) system, ethanol-induced hyperactivity might provide a screening model to investigate the effect of ethanol on reward pathways [15].
• A further suppression of ethanol-induced hyperactivity was reached by pretreatment with aminooxyacetic acid (AOAA, 15 mg/kg i.p.). The stimulation of motor activity induced by morphine (10 mg/kg i.p.) remained unaffected by even high doses of i.p. GABA [16].
• Effect of taurine on ethanol-induced changes in open-field locomotor activity [17].
• In mice pretreated with 40 mg/kg caffeine potentiation of ethanol-induced ataxia was observed only at 20 min after ethanol [18].

Biological context of Etohi1

• Ethanol-induced intracellular calcium mobilization rapidly alters gene expression in the mouse blastocyst [19].
• 1-Octanol and related compounds may prove useful in dissecting the role of altered cell adhesion in ethanol-induced injury of the nervous system [20].
• Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain [21].
• In conclusion, these data support the hypotheses that hepatocellular oxidative stress leads to cell death and that TNFalpha-induced Ras activation is important in hepatic proliferation in response to ethanol-induced liver injury [22].
• Ethanol-induced cell sensitization to bleomycin cytotoxicity produced a decrease in cell survival which became dependent on dose and time of drug treatment [23].

Anatomical context of Etohi1

• Inhibition of Ras with adenovirus containing a dominant-negative Ras had no effect on ethanol-induced liver injury, but significantly blunted ethanol-induced hepatocyte proliferation by more than 50% [22].
• We previously reported a link between ethanol-induced elevation of homocysteine, endoplasmic reticulum (ER) stress, and alcoholic liver injury in the murine model of intragastric ethanol feeding [24].
• Hybridomas were prepared from mouse myeloma cells and spleen cells derived from female BALB/c mice that had been immunized with a partially purified ethanol-induced rat liver cytochrome P-450 (P-450et) [25].
• Pretreatment of membranes with pertussis toxin reversed the ethanol-induced inhibition in adenylylcyclase activity [26].
• Ethanol-induced oxidative stress is important in the regulation of transcription factor activation and cytokine production by Kupffer cells [27].

Associations of Etohi1 with chemical compounds

• Ethanol-induced mitochondrial DNA depletion was prevented by 4-methylpyrazole, an inhibitor of ethanol metabolism, and attenuated by melatonin, an antioxidant [28].
• Betaine did not attenuate the ethanol-induced increase in tumor necrosis factor alpha or CD14 mRNA [29].
• Cytochrome P450 CYP2E1, but not nicotinamide adenine dinucleotide phosphate oxidase, is required for ethanol-induced oxidative DNA damage in rodent liver [30].
• Ethanol-induced cell sensitization to bleomycin cytotoxicity and the inhibition of recovery from potentially lethal damage [23].
• Thus, the observed ethanol-induced reduction in RA may be caused by ethanol inhibition of retinol oxidation catalyzed by class IV ADH [31].

Physical interactions of Etohi1

• Effect of leptin administration on membrane-bound adenosine triphosphatase activity in ethanol-induced experimental liver toxicity [32].

Enzymatic interactions of Etohi1

• We previously proposed an hypothesis that fetal alcohol syndrome is caused by an ethanol-induced inhibition of retinoic acid synthesis catalyzed by alcohol dehydrogenase (ADH) [33].

Regulatory relationships of Etohi1

• In reconstituted systems containing phospholipid and NADPH-cytochrome P-450 reductase, MAb 1-91-3 inhibited aniline p-hydroxylase activity of purified ethanol-induced P-450et and acetone-induced P-450 by more than 90% [25].
• Overexpression of a wild-type RAX dramatically enhanced sensitivity to ethanol-induced PKR/eIF2alpha phosphorylation, as well as translational inhibition and cell death [34].
• Knockout of the alpha7 nAChR gene selectively enhanced ethanol-induced neurotoxicity in a gene dosage-related fashion [35].
• Ethanol-induced hypothermia in wild-type control mice was significantly reduced in PACAP-deficient mice [36].
• AC1 and AC8 are expressed widely throughout the brain of neonatal mice, and genetic deletion of both AC1 and AC8 in double-knock-out (DKO) mice enhances ethanol-induced neurodegeneration in the brains of neonatal mice [37].

Other interactions of Etohi1

• However, in mice deficient in the receptor-type 1 for TNFalpha (TNFR1(-/-)), ethanol-induced liver injury and the increase in Ras activity were significantly blunted compared with wild-type mice [22].
• Genetic factors influence ethanol-induced uroporphyria in Hfe(-/-) mice [38].
• Ethanol-induced sleep was significantly longer only in Adh1 -/- mice [39].
• Hydrogen peroxide formation and actin filament reorganization by Cdc42 are essential for ethanol-induced in vitro angiogenesis [40].
• Metallothionein-knockout and wild-type 129/Sv mice were pair-fed an ethanol-containing liquid diet for 12 weeks, and the effects of zinc supplementation on ethanol-induced liver injury were analyzed [41].

Analytical, diagnostic and therapeutic context of Etohi1

• Capsaicin (160 micro M) together with intragastric perfusion of beraprost sodium (PGI(2) analogue, 2.5 micro g/ml) showed enhanced protection against ethanol induced injury [42].
• The opposite effect of ibuprofen on ethanol-induced cognitive impairment as measured by two lateralized functions is consistent with the reports in tissue and animal models that central nervous system effects of ethanol may be mediated at least in part by prostaglandins [43].
• Northern blot hybridization verified ethanol-induced increases in mRNA abundance for five cDNA clones isolated from ethanol-treated NG108-15 neuroblastoma x glioma cells [44].
• RATIONALE: GABA(A) receptor antagonists have been shown to reduce ethanol self-administration and ethanol-induced conditioned taste aversion (CTA) in rats, suggesting a role for the GABA(A) receptor in modulating ethanol's motivational effects [45].
• After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice [46].

References