ArticleInternational journal of molecular sciences2022
Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Benzothiazepane-Based Curcumin Analogs Show Selective Effects on Respiration, Permeability, and Growth of Gut-Liver (Co-Culture) Cell Models.Chemical biology & drug design · 2026Article
- Purinergic and Energy Metabolism Disruption in Oxidative Stress-Mediated Immunotoxicity Induced by Aflatoxin BJournal of fungi (Basel, Switzerland) · 2026Article
- CRISPR/Cas9-Mediated Knockout of CGNL1 Confers Resistance to Aflatoxin B1 in Porcine Intestinal Epithelial Cells via Suppressing ROS Generation.International journal of molecular sciences · 2026Article
- Fumonisin BEpigenetics · 2025Article
- Mechanism of fumonisin B1 on growth performance and intestinal structural integrity of juvenile grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- Food Iminosugars and Related Synthetic Derivatives Shift Energy Metabolism and Induce Structural Changes in Colon Cancer Cell Lines.Foods (Basel, Switzerland) · 2025Article
- Article
- Current Knowledge of Individual and Combined Toxicities of Aflatoxin B1 and Fumonisin B1 In Vitro.Toxins · 2023Review
- The Preferential Therapeutic Potential ofToxins · 2022Article
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
No grant is acknowledged in the PubMed record.
Abstract
Fumonisin B1 (FB1) and aflatoxin B1 (AFB1) are frequent contaminants of staple foods such as maize. Oral exposure to these toxins poses health hazards by disrupting cellular signaling. However, little is known regarding the multifaced mitochondrial dysfunction-linked toxicity of FB1 and AFB1. Here, we show that after exposure to FB1 and AFB1, mitochondrial respiration significantly decreased by measuring the oxygen consumption rate (OCR), mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). The current work shows that the integrity of mitochondria (MMP and ROS), that is the central component of cell apoptosis, is disrupted by FB1 and AFB1 in undifferentiated Caco-2 and HepG2 cells as in vitro models for human intestine and liver, respectively. It hypothesizes that FB1 and AFB1 could disrupt the mitochondrial electron transport chain (ETC) to induce mitochondrial dysfunction and break the balance of transferring H
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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.