Ferroptosis in Mycotoxin-Induced Toxicity: Molecular Mechanisms, Intervention Implications, and Future Directions
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View abstract on PubMed
Summary
This summary is machine-generated.Mycotoxins trigger ferroptosis, a cell death pathway, leading to systemic toxicity in humans and animals. Natural compounds and nutrients can counteract this mycotoxin-induced ferroptosis, offering protective health strategies.
Area Of Science
- Toxicology
- Cell Biology
- Biochemistry
Background
- Chronic exposure to mycotoxins in food and feed causes toxicity in humans and animals.
- Ferroptosis, a regulated cell death pathway, is increasingly recognized as a key mechanism in mycotoxin-induced pathology.
- Mycotoxins disrupt cellular processes including iron metabolism, lipid peroxidation, and antioxidant systems.
Purpose Of The Study
- To systematically review the role of ferroptosis in mycotoxin toxicity.
- To elucidate the molecular pathways and regulatory networks involved in mycotoxin-induced ferroptosis.
- To identify potential therapeutic interventions against mycotoxin-induced ferroptosis.
Main Methods
- Systematic literature review of studies on mycotoxins and ferroptosis.
- Analysis of molecular mechanisms linking mycotoxins to ferroptosis.
- Evaluation of natural compounds and nutrients as counteracting agents.
Main Results
- Key mycotoxins (e.g., deoxynivalenol, aflatoxin B1) induce ferroptosis via iron dysregulation, lipid accumulation, and impaired antioxidant defenses (GPX4, FSP1).
- Ferroptosis impacts organ-specific and systemic toxicity.
- Natural compounds (polyphenols), selenium, prebiotics, melatonin, and L-fucose mitigate mycotoxin-induced ferroptosis.
Conclusions
- Ferroptosis is a critical mediator of chronic mycotoxin toxicity.
- Interventions targeting ferroptosis, including natural products, show promise for protecting human and animal health.
- Further research is needed to develop a ferroptosis-centric framework for mycotoxin risk management.
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