ArticleNature communications2022
Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- Biomarkers for Alzheimer's disease across diverse biological domains: an umbrella review and evidence map.Journal of advanced research · 2026Pooled it
- Effects of GSH on Alcohol Metabolism and Hangover Improvement in Humans: A Randomized Double-Blind Placebo-Controlled Crossover Clinical Trial.Nutrients · 2024Trial
- A novel role for transcription factor NFE2 in redox regulation and chemotherapy resistance in acute myeloid leukemia.Leukemia · 2026Article
- Process-integrated engineered resting cells for biocatalytic production of rare natural sugars from sole methanol molecules.Nature communications · 2026Article
- Aldehyde Detoxification in Cancer: Metabolic Guardians of the Genome.Biomolecules · 2026Review
- Oxidative stress causes a reversible decrease of deubiquitylases activity in old vertebrate brains.Nature communications · 2026Article
- Role of Trichostatin A (TSA) in modulating the epigenetic modification in the lymphocytes of colorectal cancer (CRC).Clinical epigenetics · 2025Article
- Prebiotic Roles of Formaldehyde as an Activating Agent and a Building Block in Solid-State Peptide Modification.ACS bio & med chem Au · 2025Article
- Genotoxic formaldehyde and lipid aldehydes are sources of DNA damage in keratinocytes.bioRxiv : the preprint server for biology · 2025Article
- Mechanistic insights into alcohol-induced DNA crosslink repair by Slx4-Xpf-Ercc1 nuclease complex in the Fanconi anaemia pathway.Communications biology · 2025Article
- Proteomic Characterization of the Rhesus Macaque Lens Nucleus: Similarity to Human Lens, Age Effects on Protein Solubility, and Trends in Post-Translational Modifications.Investigative ophthalmology & visual science · 2025Article
- Article
- Expression of Aldehyde Dehydrogenase 1A1 in Relapse-Associated Cells in Acute Myeloid Leukemia.Cells · 2025Review
- ALDH9A1 deficiency as a source of endogenous DNA damage that requires repair by the Fanconi anemia pathway.The Journal of cell biology · 2025Article
- Investigating the origins of the mutational signatures in cancer.Nucleic acids research · 2025Review
- Naphthalimide-based fluorescent polymeric probe: a dual-phase sensor for formaldehyde detection.Science and technology of advanced materials · 2025Article
- Effect of gentiopicroside on endogenous formaldehyde homocysteine-pathway related proteins in rats with non-alcoholic steatohepatitis.Frontiers in pharmacology · 2025Article
- Toxicity of formaldehyde, and its role in the formation of harmful and aromatic compounds during food processing.Food chemistry: X · 2025Review
- Gene acquisition by giant transposons primes eukaryotes for rapid evolution via horizontal gene transfer.Science advances · 2024Article
- Exogenous and endogenous formaldehyde-induced DNA damage in the aging brain: mechanisms and implications for brain diseases.Cell biology and toxicology · 2024Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Formaldehyde (FA) is a ubiquitous endogenous and environmental metabolite that is thought to exert cytotoxicity through DNA and DNA-protein crosslinking, likely contributing to the onset of the human DNA repair condition Fanconi Anaemia. Mutations in the genes coding for FA detoxifying enzymes underlie a human inherited bone marrow failure syndrome (IBMFS), even in the presence of functional DNA repair, raising the question of whether FA causes relevant cellular damage beyond genotoxicity. Here, we report that FA triggers cellular redox imbalance in human cells and in Caenorhabditis elegans. Mechanistically, FA reacts with the redox-active thiol group of glutathione (GSH), altering the GSH:GSSG ratio and causing oxidative stress. FA cytotoxicity is prevented by the enzyme alcohol dehydrogenase 5 (ADH5/GSNOR), which metabolizes FA-GSH products, lastly yielding reduced GSH. Furthermore, we show that GSH synthesis protects human cells from FA, indicating an active role of GSH in preventing FA toxicity. These findings might be relevant for patients carrying mutations in FA-detoxification systems and could suggest therapeutic benefits from thiol-rich antioxidants like N-acetyl-L-cysteine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.