ReviewArchives of toxicology2021
Hypoxia, oxidative stress, and immune evasion: a trinity of the trichothecenes T-2 toxin and deoxynivalenol (DON).
Review in Archives of toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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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
23 citing papers in PubMed, 71 citations in OpenAlex.
- An investigation into the cellular-level adverse effects of tourniquet use on the infrapatellar fat pad in primary total knee arthroplasty: A prospective randomized study.Acta orthopaedica et traumatologica turcica · 2023Trial
- Lycopene mitigates T-2 toxin-induced systemic inflammation and oxidative stress in association with gut microbiota and SCFAs regulation in mice.Stress biology · 2026Article
- Proteomic analysis reveals the molecular mechanisms of deoxynivalenol-induced injury in the jejunum of piglets.BMC genomics · 2026Article
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- Mitochondrial DNA Mutations as a Factor in the Heritability of Atherosclerosis and Other Diseases.Current medicinal chemistry · 2025Review
- Review
- Uridine diphosphate glucuronosyltransferase 1A1 prevents the progression of liver injury.World journal of gastroenterology · 2024Article
- Review of neurotoxicity of T-2 toxin.Mycotoxin research · 2024Review
- Involvement of Yes-Associated Protein 1 Activation in the Matrix Degradation of Human-Induced-Pluripotent-Stem-Cell-Derived Chondrocytes Induced by T-2 Toxin and Deoxynivalenol Alone and in Combination.International journal of molecular sciences · 2024Article
- A hypoxia-related genes prognostic risk model, and mechanisms of hypoxia contributing to poor prognosis through immune microenvironment and drug resistance in acute myeloid leukemia.Frontiers in pharmacology · 2024Article
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- Article
- Influence of deoxynivalenol and zearalenone on the immunohistochemical expression of oestrogen receptors and liver enzyme genes in vivo in prepubertal gilts.Archives of toxicology · 2023Article
- Article
- The Multidirectional Influence of Feed-Borne Deoxynivalenol and Zearalenone on Animal Health.Toxins · 2023Article
- A comprehensive analysis of the hub genes for oxidative stress in ischemic stroke.Frontiers in neuroscience · 2023Article
- Article
- Article
- Analysis ofInternational journal of molecular sciences · 2022Article
- Identification of NewInternational journal of environmental research and public health · 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
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-2 toxin and deoxynivalenol (DON) are type A and B trichothecenes, respectively. They widely occur as pollutants in food and crops and cause a series of toxicities, including immunotoxicity, hepatotoxicity, and neurotoxicity. Oxidative stress is the primary mechanistic basis of these toxic effects. Increasing amounts of evidence have shown that mitochondria are significant targets of apoptosis caused by T-2 toxin- and DON-induced oxidative stress via regulation of Bax/B-cell lymphoma-2 and caspase-3/caspase-9 signaling. DNA methylation and autophagy are involved in oxidative stress related to apoptosis, and hypoxia and immune evasion are related to oxidative stress in this context. Hypoxia induces oxidative stress by stimulating mitochondrial reactive oxygen species production and regulates the expression of cytokines, such as interleukin-1β and tumor necrosis factor-α. Programmed cell death-ligand 1 is upregulated by these cytokines and by hypoxia-inducible factor-1, which allows it to bind to programmed cell death-1 to enable escape of immune cell surveillance and achievement of immune evasion. This review concentrates on novel findings regarding the oxidative stress mechanisms of the trichothecenes T-2 toxin and DON. Importantly, we discuss the new evidence regarding the connection of hypoxia and immune evasion with oxidative stress in this context. Finally, the trinity of hypoxia, oxidative stress and immune evasion is highlighted. This work will be conducive to an improved understanding of the oxidative stress caused by trichothecene mycotoxins.
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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.