Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of alcohol elimination is highly resistant to acceleration in vivo in well-nourished individuals. The acceleration of ethanol elimination may be achieved by providing the conditions in which the action of alcohol dehydrogenase is not delayed by the insufficiency of the oxidized NAD form. The aim of the study was to verify the theoretically assumed mechanism of accelerating alcohol elimination by administering excessive acetoacetate (Ac-Ac) in the experimental in vitro model. Ac-Ac forming the redox system with beta-hydroxybutyrate (beta-HBA) is the natural acceptor of excessive protons from ethanol oxidation. Ac-Ac and beta-HBA penetrate freely through the cell membranes and are easily assimilated energetic substrates. The examinations were performed using the hepatic homogenates (collected from the cadavers shortly after death) supplemented with ethanol and Ac-Ac. The ethanol levels were determined at 0, 15, 60, 90 and 150 min of the experiment. The findings showed that the equimolar addition of Ac-Ac resulted in a two- to three-fold increase in ethanol oxidation in hepatic homogenates. The biochemical system discussed above resembles the natural way of utilizing the excessive NADH, which is formed during ethanol combustion in chronic alcoholics. The results indicate that further investigations are necessary to assess the clinical importance of this metabolic system.
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PMID:In vitro co-metabolism of acetoacetate and ethanol in human hepatic mitochondrial and cytosolic fractions. 1617 17

Methanol (MeOH) is considered to be a poison in humans because of the alcohol dehydrogenase (ADH)-mediated conversion of MeOH to formaldehyde (FA), which is toxic. Our recent genome-wide analysis of the mouse brain demonstrated that an increase in endogenous MeOH after ADH inhibition led to a significant increase in the plasma MeOH concentration and a modification of mRNA synthesis. These findings suggest endogenous MeOH involvement in homeostasis regulation by controlling mRNA levels. Here, we demonstrate directly that study volunteers displayed increasing concentrations of MeOH and FA in their blood plasma when consuming citrus pectin, ethanol and red wine. A microarray analysis of white blood cells (WBC) from volunteers after pectin intake showed various responses for 30 significantly differentially regulated mRNAs, most of which were somehow involved in the pathogenesis of Alzheimer's disease (AD). There was also a decreased synthesis of hemoglobin mRNA, HBA and HBB, the presence of which in WBC RNA was not a result of red blood cells contamination because erythrocyte-specific marker genes were not significantly expressed. A qRT-PCR analysis of volunteer WBCs after pectin and red wine intake confirmed the complicated relationship between the plasma MeOH content and the mRNA accumulation of both genes that were previously identified, namely, GAPDH and SNX27, and genes revealed in this study, including MME, SORL1, DDIT4, HBA and HBB. We hypothesized that human plasma MeOH has an impact on the WBC mRNA levels of genes involved in cell signaling.
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PMID:Dietary methanol regulates human gene activity. 2503 51