ArticleJournal of advanced research2025
Mechanistic insights into ferroptosis and apoptosis pathways: Synergistic effects of multi-organ toxicity and transgenerational effects induced by co-exposure of epoxiconazole and aflatoxin B1 in zebrafish.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Quercetin ameliorates aflatoxin BJournal of animal science and biotechnology · 2026Article
- Biocontrol of Mycotoxin-Producing Fungi by Lactic Acid Bacteria.Foods (Basel, Switzerland) · 2026Review
- Aflatoxins and Human Health: Global Exposure, Disease Burden, and One Health Strategies.Toxins · 2026Review
- Mycotoxin Contamination: Occurrence, Biotransformation, Pathogenic Mechanisms, and Strategies for Nutritional Intervention.Molecules (Basel, Switzerland) · 2025Review
- Impact of Aflatoxins on the Digestive, Immune, and Nervous Systems: The Role of Microbiota and Probiotics in Toxicity Protection.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionIn the environment, mycotoxins and fungicides frequently coexist, potentially causing synergistic risks to organisms. Epoxiconazole (EPO) and aflatoxin B1 (AFB1) are a common fungicide and mycotoxins, respectively, which are widely present in the environment and have toxic effects on multiple organs once entering the organism, but it is still unclear whether the co-exposure has a synergistic toxic effect.
objectivesThis study delves into the molecular mechanisms underlying the co-exposure to EPO and AFB1, emphasizing multi-organ toxicity in female zebrafish (F0 generation) and potential transgenerational impacts on the offspring embryos (F1 generation) through multi-omics approaches.
resultsFindings indicate that exposure to either EPO or AFB1, individually or combined, intensified intestinal pathological damage, decreased the expression of tight junction proteins, altered gut microbiota composition, and induced intestinal inflammation, with co-exposure causing more severe effects. RNA-seq analysis revealed an enrichment of ferroptosis and apoptosis pathways in the liver and ovaries of F0 zebrafish. Co-exposure markedly altered the expression of associated molecules, exacerbating pathological damage in these organs. Molecular docking studies revealed that AFB1 exhibited lower binding energies to Caspase3, GPX4 and IL-1β compared to EPO, suggesting that it may have a higher binding capacity. Furthermore, both single and combined exposures modified the expression of molecules related to apoptosis, inflammatory response, and ferroptosis in unexposed F1 embryos, with co-exposure demonstrating more significant biological effects, thereby confirming transgenerational toxicity.
conclusionThe present study provides preliminary evidence on the potential mechanisms of combined exposure-induced multi-organ toxicity, highlighting ferroptosis of the liver and apoptosis of the ovary as key pathways. These findings provide new perspectives and methods for risk assessment of multiple environmental pollutants.
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