ArticleFrontiers in behavioral neuroscience2013
Gene specific modifications unravel ethanol and acetaldehyde actions.
Article in Frontiers in behavioral neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Genome-wide association discoveries of alcohol dependence.The American journal on addictionsPooled it
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- Peripheral alcohol metabolism dictates ethanol consumption and drinking microstructure in mice.Alcohol, clinical & experimental research · 2025Article
- Hepatic progesterone receptor membrane component 1 attenuates ethanol-induced liver injury by reducing acetaldehyde production and oxidative stress.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Adult-onset hypothyroidism increases ethanol consumption.Psychopharmacology · 2019Article
- Intravenous self-administration of alcohol in rats-problems with translation to humans.Addiction biology · 2017Review
- Acquisition, Maintenance and Relapse-Like Alcohol Drinking: Lessons from the UChB Rat Line.Frontiers in behavioral neuroscience · 2017Review
- On the Accuracy ofFrontiers in behavioral neuroscience · 2017Review
- Quantification of Neural Ethanol and Acetaldehyde Using Headspace GC-MS.Alcoholism, clinical and experimental research · 2016Article
- Hairpin Ribozyme Genes Curtail Alcohol Drinking: from Rational Design to in vivo Effects in the Rat.Molecular therapy. Nucleic acids · 2016Article
- Genetic and Environmental Predictors of Alcohol Use in Asian American Young Adults.Journal of studies on alcohol and drugs · 2015Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ethanol is metabolized into acetaldehyde mainly by the action of alcohol dehydrogenase in the liver, while mainly by the action of catalase in the brain. Aldehyde dehydrogenase-2 metabolizes acetaldehyde into acetate in both organs. Gene specific modifications reviewed here show that an increased liver generation of acetaldehyde (by transduction of a gene coding for a high-activity liver alcohol dehydrogenase ADH1(*)B2) leads to increased blood acetaldehyde levels and aversion to ethanol in animals. Similarly aversive is an increased acetaldehyde level resulting from the inhibition of liver aldehyde dehydrogenase-2 (ALDH2) synthesis (by an antisense coding gene against aldh2 mRNA). The situation is diametrically different when acetaldehyde is generated in the brain. When the brain ventral tegmental area (VTA) is endowed with an increased ability to generate acetaldehyde (by transfection of liver rADH) the reinforcing effects of ethanol are increased, while a highly specific inhibition of catalase synthesis (by transduction of a shRNA anti catalase mRNA) virtually abolishes the reinforcing effects of ethanol as seen by a complete abolition of ethanol intake in rats bred for generations as high ethanol drinkers. Data shows two divergent effects of increases in acetaldehyde generation: aversive in the periphery but reinforcing in the brain.
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