ArticleFrontiers in toxicology2025
Acetaldehyde and methylglyoxal: comparative analysis of toxic electronic cigarette degradation products in 3D and 2D exposure systems using human bronchial epithelial models.
Article in Frontiers in toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Background: Acetaldehyde and methylglyoxal are structurally related aldehydes produced by thermal degradation of the electronic cigarette (EC) solvents, propylene glycol and glycerin. Despite their presence in EC aerosols, the biological effects of these aldehydes when inhaled during vaping are largely unknown. Methods: Three-dimensional (3D) human bronchial epithelial tissues (EpiAirway™) were exposed at the air liquid interface (ALI) to aerosols containing acetaldehyde or methylglyoxal at concentrations relevant to human vaping. PBS-exposed tissues served as controls. Comparative proteomic analyses were performed to assess global alterations in protein expression. Based on proteomics data, concentration-response experiments were conducted using BEAS-2B bronchial epithelial cells to evaluate reactive oxygen species, mitochondrial function, and cytoskeletal integrity. Results: ALI exposure to acetaldehyde or methylglyoxal resulted in 79 and 76 differentially expressed proteins (DEPs), respectively, with 51 overlapping proteins exhibiting similar fold change directionality. Ingenuity Pathway Analysis (IPA) Toxicity Lists identified key affected pathways, including mitochondrial dysfunction, fatty acid metabolism, G2/M DNA damage checkpoint regulation, and mitochondrial biogenesis. Gene Ontology (GO) ontology analysis revealed substantial overlap in affected biological processes and cellular components. Findings were further supported and expanded in BEAS-2B cell concentration-response assays, which confirmed mitochondrial impairment, elevated ROS levels, and disrupted cytoskeletal organization. Notably, TRPM8 inhibition attenuated methylglyoxal-induced mitochondrial dysfunction (MTT assay), while both TRPM8 and TRPA1 inhibition partially rescued actin depolymerization. Conclusion: Brief ALI exposure of EpiAirway™ tissues to vaping-relevant concentrations of acetaldehyde or methylglyoxal altered the bronchial epithelial proteome. Complementary concentration-response experiments with submerged BEAS-2B cells confirmed and extended the proteomics data. While both aldehydes exhibited similar proteomic and functional impacts, methylglyoxal was effective at substantially lower concentrations in all assays with some effects partially mediated via TRPA1 and TRPM8 channels.
Indexed as
Identifiers
What OpenQuestion holds
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.