Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (651 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A colorless, flammable liquid used in the manufacture of acetic acid, perfumes, and flavors. It is also an intermediate in the metabolism of alcohol. It has a general narcotic action and also causes irritation of mucous membranes. Large doses may cause death from respiratory paralysis.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Ethanal.
Where it fits in the MeSH classification
- Broader topics
- Aldehydes
- Narrower topics
- Paraldehyde
Research landscape
PubMed indexes 6,908 records tagged with the MeSH heading “Acetaldehyde” (counts retrieved 2026-10-31). 634 of them (9.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,856 records.
Reviews account for 471 records (6.8%) and meta-analyses for 4. Randomized controlled trials number 51 (0.7%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,856 |
| 2000-2009 | 1,296 |
| 2010-2019 | 1,122 |
| 2020 onward | 634 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 471 | 6.8% |
| Meta-analyses | 4 | 0.1% |
| Randomized controlled trials | 51 | 0.7% |
Method: PubMed query "Acetaldehyde"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Constructing a synthetic pathway for acetyl-coenzyme A from one-carbon through enzyme design | 2019 | Research article Design not recorded in structured metadata | 146 | cc by PMID 30914637 · DOI · PMC6435721 |
| Alcohol and acetaldehyde in public health: from marvel to menace | 2010 | Review article Design not recorded in structured metadata | 111 | cc by PMID 20617031 · DOI · PMC2872347 |
| Molecular Mechanisms of Acetaldehyde-Mediated Carcinogenesis in Squamous Epithelium | 2017 | Review article Design not recorded in structured metadata | 93 | cc by PMID 28891965 · DOI · PMC5618592 |
| Acetaldehyde-driven mRNA methylation and expression changes in ethanol-metabolizing enzyme genes | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 40252050 · DOI · PMC12013419 |
Constructing a synthetic pathway for acetyl-coenzyme A from one-carbon through enzyme design [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Acetyl-CoA is a fundamental metabolite for all life on Earth, and is also a key starting point for the biosynthesis of a variety of industrial chemicals and natural products.
- Closing excerpt
- The SACA pathway is proved to be the shortest, ATP-independent, carbon-conserving and oxygen-insensitive pathway for acetyl-CoA biosynthesis, opening possibilities for producing acetyl-CoA-derived chemicals from one-carbon resources in the future.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Acetyl-CoA is a fundamental metabolite for all life on Earth, and is also a key starting point for the biosynthesis of a variety of industrial chemicals and natural products. Here we design and construct a Synthetic Acetyl-CoA (SACA) pathway by repurposing glycolaldehyde synthase and acetyl-phosphate synthase. First, we design and engineer glycolaldehyde synthase to improve catalytic activity more than 70-fold, to condense two molecules of formaldehyde into one glycolaldehyde. Second, we repurpose a phosphoketolase to convert glycolaldehyde into acetyl-phosphate. We demonstrated the feasibility of the SACA pathway in vitro, achieving a carbon yield ~50%, and confirmed the SACA pathway by 13C-labeled metabolites. Finally, the SACA pathway was verified by cell growth using glycolaldehyde, formaldehyde and methanol as supplemental carbon source. The SACA pathway is proved to be the shortest, ATP-independent, carbon-conserving and oxygen-insensitive pathway for acetyl-CoA biosynthesis, opening possibilities for producing acetyl-CoA-derived chemicals from one-carbon resources in the future.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30914637 · DOI · PMC6435721
Alcohol and acetaldehyde in public health: from marvel to menace [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Alcohol abuse is a serious medical and social problem.
- Closing excerpt
- Meanwhile, free radicals produced during ethanol metabolism and FAEEs are also important triggers for alcoholic damages.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (108 words)
Alcohol abuse is a serious medical and social problem. Although light to moderate alcohol consumption is beneficial to cardiovascular health, heavy drinking often results in organ damage and social problems. In addition, genetic susceptibility to the effect of alcohol on cancer and coronary heart disease differs across the population. A number of mechanisms including direct the toxicity of ethanol, its metabolites [e.g., acetaldehyde and fatty acid ethyl esters (FAEEs)] and oxidative stress may mediate alcoholic complications. Acetaldehyde, the primary metabolic product of ethanol, is an important candidate toxin in developing alcoholic diseases. Meanwhile, free radicals produced during ethanol metabolism and FAEEs are also important triggers for alcoholic damages.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20617031 · DOI · PMC2872347
Molecular Mechanisms of Acetaldehyde-Mediated Carcinogenesis in Squamous Epithelium [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Acetaldehyde is a highly reactive compound that causes various forms of damage to DNA, including DNA adducts, single- and/or double-strand breaks (DSBs), point mutations, sister chromatid exchanges (SCEs), and DNA-DNA cross-links.
- Closing excerpt
- We also give attention to research on acetaldehyde-mediated DNA repair pathways such as the Fanconi anemia pathway and refer to our studies on the prevention of acetaldehyde-mediated DNA damage.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (194 words)
Acetaldehyde is a highly reactive compound that causes various forms of damage to DNA, including DNA adducts, single- and/or double-strand breaks (DSBs), point mutations, sister chromatid exchanges (SCEs), and DNA-DNA cross-links. Among these, DNA adducts such as N²-ethylidene-2'-deoxyguanosine, N²-ethyl-2'-deoxyguanosine, N²-propano-2'-deoxyguanosine, and N²-etheno-2'-deoxyguanosine are central to acetaldehyde-mediated DNA damage because they are associated with the induction of DNA mutations, DNA-DNA cross-links, DSBs, and SCEs. Acetaldehyde is produced endogenously by alcohol metabolism and is catalyzed by aldehyde dehydrogenase 2 (ALDH2). Alcohol consumption increases blood and salivary acetaldehyde levels, especially in individuals with ALDH2 polymorphisms, which are highly associated with the risk of squamous cell carcinomas in the upper aerodigestive tract. Based on extensive epidemiological evidence, the International Agency for Research on Cancer defined acetaldehyde associated with the consumption of alcoholic beverages as a "group 1 carcinogen" (definite carcinogen) for the esophagus and/or head and neck. In this article, we review recent advances from studies of acetaldehyde-mediated carcinogenesis in the squamous epithelium, focusing especially on acetaldehyde-mediated DNA adducts. We also give attention to research on acetaldehyde-mediated DNA repair pathways such as the Fanconi anemia pathway and refer to our studies on the prevention of acetaldehyde-mediated DNA damage.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28891965 · DOI · PMC5618592
Acetaldehyde-driven mRNA methylation and expression changes in ethanol-metabolizing enzyme genes [4]
Abstract reading summary — source excerpts
- Opening excerpt
- This study examines how the alcohol metabolite acetaldehyde modulates mRNA methylation and expression of ethanol-metabolizing genes, uncovering its epigenetic role in ethanol metabolism.
- Closing excerpt
- These findings highlight the cell-specific epigenetic effects of acetaldehyde, particularly its role in modulating mRNA methylation and expression of ALDH2, a key enzyme in alcohol metabolism.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
This study examines how the alcohol metabolite acetaldehyde modulates mRNA methylation and expression of ethanol-metabolizing genes, uncovering its epigenetic role in ethanol metabolism. Using neuron-like (SH-SY5Y) and non-neuronal (SW620) cellular models, we examined the effects of chronic intermittent acetaldehyde (CIA) exposure and subsequent withdrawal (CIA+WD) on global RNA m6A modifications and the methylation and expression of three brain ethanol-metabolizing genes: CAT (catalase), CYP2E1 (cytochrome P450 2E1), and ALDH2 (aldehyde dehydrogenase 2). A 3-week CIA exposure, with or without 24-hour withdrawal, did not significantly alter global m6A methylation levels in either cell line. However, acetaldehyde exposure/withdrawal induced hypermethylation at the mRNA stop codon regions of ALDH2 (CIA: p = 0.002; CIA+WD: p = 0.055) and CAT (CIA: p = 0.077; CIA+WD: p = 0.036) in SH-SY5Y cells, but not in SW620 cells. Furthermore, ALDH2 mRNA expression was significantly upregulated in both cell types following exposure (SH-SY5Y: p = 0.073 [CIA] and 0.00002 [CIA+WD]; SW620: p = 0.0009 [CIA] and 0.00008 [CIA+WD]). In contrast, CYP2E1 mRNA methylation and the expression of CYP2E1 and CAT remained unchanged. These findings highlight the cell-specific epigenetic effects of acetaldehyde, particularly its role in modulating mRNA methylation and expression of ALDH2, a key enzyme in alcohol metabolism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40252050 · DOI · PMC12013419
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article A review of the pharmacokinetics and pharmacodynamics of disulfiram and its metabolites [5]
- Research article DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis [6]
- Research article Acetaldehyde adducts in alcoholic liver disease [7]
- Research article Cytotoxic fungi--an overview [8]
- Research article Radical mechanisms of enzymatic catalysis [9]
- Research article Role of malondialdehyde-acetaldehyde adducts in liver injury [10]
References
- Lu X, Liu Y, Yang Y, Wang S, Wang Q, Wang X, et al.. Constructing a synthetic pathway for acetyl-coenzyme A from one-carbon through enzyme design. . 2019. PMID 30914637 · DOI · PMC6435721
- Guo R, Ren J. Alcohol and acetaldehyde in public health: from marvel to menace. . 2010. PMID 20617031 · DOI · PMC2872347
- Mizumoto A, Ohashi S, Hirohashi K, Amanuma Y, Matsuda T, Muto M. Molecular Mechanisms of Acetaldehyde-Mediated Carcinogenesis in Squamous Epithelium. . 2017. PMID 28891965 · DOI · PMC5618592
- Koo JS, Zhan Q, Zhang H. Acetaldehyde-driven mRNA methylation and expression changes in ethanol-metabolizing enzyme genes. . 2025. PMID 40252050 · DOI · PMC12013419
- Johansson B. A review of the pharmacokinetics and pharmacodynamics of disulfiram and its metabolites. Acta Psychiatr Scand Suppl. 1992. PMID 1471547 · DOI
- Brooks PJ, Theruvathu JA. DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis. Alcohol. 2005. PMID 16054980 · DOI
- Setshedi M, Wands JR, Monte SM. Acetaldehyde adducts in alcoholic liver disease. Oxid Med Cell Longev. 2010. PMID 20716942 · DOI · PMC2952076
- Karlson-Stiber C, Persson H. Cytotoxic fungi--an overview. Toxicon. 2003. PMID 14505933 · DOI
- Frey PA. Radical mechanisms of enzymatic catalysis. Annu Rev Biochem. 2001. PMID 11395404 · DOI
- Tuma DJ. Role of malondialdehyde-acetaldehyde adducts in liver injury. Free Radic Biol Med. 2002. PMID 11841919 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.