ArticlePeerJ2019
Metabolomic analysis reveals the mechanism of aluminum cytotoxicity in HT-29 cells.
Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 22 citations in OpenAlex.
- Repeated aluminum ingestion alters human intestinal structure: focus on advanced 3D tissue models.Pflugers Archiv : European journal of physiology · 2026Article
- Toward a Molecular Framework of Systemic Multi-Organ Toxicity Induced by Chronic Aluminum Chloride Exposure.Molecules (Basel, Switzerland) · 2026Review
- GC/MS-Based Metabolomic Analysis of A549 Cells Exposed to Emerging Organophosphate Flame Retardants.Toxics · 2024Article
- Effect of BiosilicateJournal of functional biomaterials · 2023Article
- Metabolomics: a promising tool for deciphering metabolic impairment in heavy metal toxicities.Frontiers in molecular biosciences · 2023Review
- Cytotoxicity and changes in gene expression under aluminium potassium sulfate on Spodoptera frugiperda 9 cells.Ecotoxicology (London, England) · 2021Article
- LC-MS Based Metabolomics Study of the Effects of EGCG on A549 Cells.Frontiers in pharmacology · 2021Article
- Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies.Advances in neurotoxicology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAluminum (Al) is toxic to animals and humans. The most common sources of human exposure to Al are food and beverages. The intestinal epithelium is the first barrier against Al-induced toxicity. In this study, HT-29, a human colon cancer cell line, was selected as an in vitro model to evaluate the Al-induced alteration in metabolomic profiles and explore the possible mechanisms of Al toxicity.
methodsMTT assay was performed to determine the half-maximal inhibitory concentration of Al ions. Liquid chromatography-mass spectrometry (LC-MS) was used for metabolomic analysis, and its results were further confirmed using quantitative reverse transcription polymerase chain reaction (RT-qPCR) of nine selected genes.
resultsAl inhibited the growth of the HT-29 cells, and its half-maximal dose for the inhibition of cell proliferation was found to be four mM. This dose was selected for further metabolomic analysis, which revealed that 81 metabolites, such glutathione (GSH), phosphatidylcholines, phosphatidylethanolamines, and creatine, and 17 metabolic pathways, such as the tricarboxylic acid cycle, pyruvate metabolism, and GSH metabolism, were significantly altered after Al exposure. The RT-qPCR results further confirmed these findings.
conclusionThe metabolomics and RT-qPCR results indicate that the mechanisms of Al-induced cytotoxicity in HT-29 cells include cellular apoptosis, oxidative stress, and alteration of lipid, energy, and amino acid metabolism.
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.