Putative Role of Brain Acetaldehyde in Ethanol Addiction
Open accessAbstract
The putative contribution of brain acetaldehyde (AcH) to ethanol (EtOH) tolerance and dependence (addiction) is reviewed. Although the role of AcH in EtOH addiction has been controversial, there are data showing a relationship. AcH can be formed in the brain tissues through the peroxidatic activity of catalase and by oxidation via other oxidizing enzymes such as cytochrome P-4502E1. Significant formation of AcH occurs in vitro in brain tissue at concentrations of EtOH that can be achieved by voluntary consumption of EtOH by rodents. AcH itself possesses reinforcing properties, which suggests that some of the behavioral pharmacological effects attributed to EtOH may be a result of the formation of AcH, and supports the involvement of AcH in EtOH addiction. Modulation of aldehyde dehydrogenase (ALDH) and brain catalase activity can change EtOH-related addictive behaviors presumably by changing AcH levels. Moreover, some condensation reaction products of AcH may promote some actions of EtOH and its consumption. On the basis of the findings, it can be concluded that AcH may mediate some of the CNS actions of EtOH including tolerance and dependence, although further exploration the involvement of AcH in EtOH addiction is warranted.
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Catalase may have a limited role in ethanol metabolism in certain brain regions, except for aminergic neurons, where it is present in high concentrations.
“However, catalase may have a limited role in ethanol metabolism in certain brain regions, except for aminergic neurons, where it is present in high concentrations134,148–150.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [148]
Mitochondrial ALDH2 is the final enzyme for converting acetaldehyde to acetate, although acetaldehyde is locally produced in the brain due to its very limited ability to cross the blood-brain barrier.
“Finally, mitochondrial ALDH2 is the final enzyme for converting acetaldehyde to acetate148, although acetaldehyde is locally produced in the brain due to its very limited ability to cross the BBB162.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [148]
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- Authors
- Deng, X.-S., & Deitrich, R.
- Affiliations
- University of Colorado Health (US)
- ORCID
- Deng, Xin-sheng
- Venue
- Current Drug Abuse Reviewse
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2008-01-01
- Volume
- 1
- Issue
- 1
- Pages
- 3-8
- ISSN
- 1874-4737 (ISSN-L)
- PMC
- PMC2613359
- OpenAlex
- W2007321017
- Cited by
- 105
- References
- 72
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 5 · 2018: 4 · 2017: 8 · 2016: 6 · 2015: 9 · 2014: 7 · 2013: 15 · 2012: 14
- FWCI
- 4.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Drug Abuse Reviews (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (AA011464, R01AA011464)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Keywords
- acetaldehyde, ethanol addiction, ethanol tolerance, ethanol dependence, catalase, CYP2E1, aldehyde dehydrogenase, ethanol reinforcement
- MeSH terms
- Aldehyde Dehydrogenase, Mitochondrial, Acetaldehyde, Ethanol, Alcoholism, Aldehyde Dehydrogenase, Animals, Brain, Catalase, Drug Tolerance, Humans, Motivation, Rodentia, Cytochrome P-450 CYP2E1
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