ArticleProceedings of the National Academy of Sciences of the United States of America2014
Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 93 citations in OpenAlex.
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- Roles of non-specific lipid transfer proteins in plant defense: structural and functional perspectives.Frontiers in fungal biology · 2025Review
- Sex-specific mitochondrial dynamics and mitophagy response to muscle damage.Physiological reports · 2022Article
- Evaluation of the Role of Probiotics As a New Strategy to Eliminate Microbial Toxins: a Review.Probiotics and antimicrobial proteins · 2022Review
- Identification of Key Pathways Involved in White Strain ofFrontiers in pharmacology · 2022Article
- Mitophagy in Yeast: Decades of Research.Cells · 2021Review
- Yeast mitophagy: Unanswered questions.Biochimica et biophysica acta. General subjects · 2021Review
- Colorectal Cancer Apoptosis Induced by Dietary δ-Valerobetaine Involves PINK1/Parkin Dependent-Mitophagy and SIRT3.International journal of molecular sciences · 2021Article
- Neuroprotection offered by mesenchymal stem cells in perinatal brain injury: Role of mitochondria, inflammation, and reactive oxygen species.Journal of neurochemistry · 2021Review
- Article
- Exploring the dermotoxicity of the mycotoxin deoxynivalenol: combined morphologic and proteomic profiling of human epidermal cells reveals alteration of lipid biosynthesis machinery and membrane structural integrity relevant for skin barrier function.Archives of toxicology · 2021Article
- A transition to degeneration triggered by oxidative stress in degenerative disorders.Molecular psychiatry · 2021Review
- The Nucleus/Mitochondria-Shuttling LncRNAs Function as New Epigenetic Regulators of Mitophagy in Cancer.Frontiers in cell and developmental biology · 2021Review
- Mitophagy Improves Ethanol Tolerance in Yeast: Regulation by Mitochondrial Reactive Oxygen Species inJournal of microbiology and biotechnology · 2020Article
- Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy.Oxidative medicine and cellular longevity · 2020Article
- Beneficial Effects of Rosmarinic Acid on IPEC-J2 Cells Exposed to the Combination of Deoxynivalenol and T-2 Toxin.Mediators of inflammation · 2020Article
- Fermented Korean Red Ginseng Extract Enriched in Rd and Rg3 Protects against Non-Alcoholic Fatty Liver Disease through Regulation of mTORC1.Nutrients · 2019Article
- LKB1/AMPK Pathway and Drug Response in Cancer: A Therapeutic Perspective.Oxidative medicine and cellular longevity · 2019Review
- Mitochondrial Dynamics: Biogenesis, Fission, Fusion, and Mitophagy in the Regulation of Stem Cell Behaviors.Stem cells international · 2019Review
- Modulators of Redox Metabolism in Head and Neck Cancer.Antioxidants & redox signaling · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trichothecene mycotoxins are natural contaminants of small grain cereals and are encountered in the environment, posing a worldwide threat to human and animal health. Their mechanism of toxicity is poorly understood, and little is known about cellular protection mechanisms against trichothecenes. We previously identified inhibition of mitochondrial protein synthesis as a novel mechanism for trichothecene-induced cell death. To identify cellular functions involved in trichothecene resistance, we screened the Saccharomyces cerevisiae deletion library for increased sensitivity to nonlethal concentrations of trichothecin (Tcin) and identified 121 strains exhibiting higher sensitivity than the parental strain. The largest group of sensitive strains had significantly higher reactive oxygen species (ROS) levels relative to the parental strain. A dose-dependent increase in ROS levels was observed in the parental strain treated with different trichothecenes, but not in a petite version of the parental strain or in the presence of a mitochondrial membrane uncoupler, indicating that mitochondria are the main site of ROS production due to toxin exposure. Cytotoxicity of trichothecenes was alleviated after treatment of the parental strain and highly sensitive mutants with antioxidants, suggesting that oxidative stress contributes to trichothecene sensitivity. Cotreatment with rapamycin and trichothecenes reduced ROS levels and cytotoxicity in the parental strain relative to the trichothecene treatment alone, but not in mitophagy deficient mutants, suggesting that elimination of trichothecene-damaged mitochondria by mitophagy improves cell survival. These results reveal that increased mitophagy is a cellular protection mechanism against trichothecene-induced mitochondrial oxidative stress and a potential target for trichothecene resistance.
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