ArticleScientific reports2017
Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 60 citations in OpenAlex.
- Hepatic cytochrome P450 induction following Kashin-Beck disease-related selenium deficiency and T-2 toxin exposure in mice.Archives of toxicology · 2026Article
- Lycopene Attenuates T2 Mycotoxin-Induced Hepatotoxicity and Dysbiosis by Activating PPAR Signaling.Biology · 2026Article
- Article
- Temporal Wheat Proteome Remodeling by Deoxynivalenol Reveals Novel Detoxification Signatures and Strategies Across Cultivars.Molecular & cellular proteomics : MCP · 2025Article
- Combined Cytotoxic Effects of the Fungicide Azoxystrobin and Common Food-Contaminating Mycotoxins.Foods (Basel, Switzerland) · 2025Article
- 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
- DNA Damage Induced by T-2 Mycotoxin in Human Skin Fibroblast Cell Line-Hs68.International journal of molecular sciences · 2023Article
- Traditional and emergingAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Impact of Deoxynivalenol and Zearalenone as Single and Combined Treatment on DNA, Cell Cycle and Cell Proliferation in HepG2 Cells.International journal of molecular sciences · 2023Article
- Article
- An integrative analysis of DNA methylation and transcriptome showed the dysfunction of MAPK pathway was involved in the damage of human chondrocyte induced by T-2 toxin.BMC molecular and cell biology · 2022Article
- Fluorine impairs carboxylesterase 1-mediated hydrolysis of T-2 toxin and increases its chondrocyte toxicity.Frontiers in nutrition · 2022Article
- Pleiotropic Roles of NOTCH1 Signaling in the Loss of Maturational Arrest of Human Osteoarthritic Chondrocytes.International journal of molecular sciences · 2021Article
- Identification of HIF-1α/VEGFA signaling pathway and transcription factors in Kashin-Beck disease by integrated bioinformatics analysis.Experimental and therapeutic medicine · 2021Article
- Hypoxia, oxidative stress, and immune evasion: a trinity of the trichothecenes T-2 toxin and deoxynivalenol (DON).Archives of toxicology · 2021Review
- Dysregulation of Cells Cycle and Apoptosis in Human Induced Pluripotent Stem Cells Chondrocytes Through p53 Pathway by HT-2 Toxin: AnFrontiers in genetics · 2021Article
- Assessing the Effect of Mycotoxin Combinations: Which Mathematical Model Is (the Most) Appropriate?Toxins · 2020Review
- Beneficial Effects of Rosmarinic Acid on IPEC-J2 Cells Exposed to the Combination of Deoxynivalenol and T-2 Toxin.Mediators of inflammation · 2020Article
- Maternal Exposure to T-2 Toxin Induces Changes in Antioxidant System and Testosterone Synthesis in the Testes of Mice Offspring.Animals : an open access journal from MDPI · 2019Article
- Deoxynivalenol Modulates the Viability, ROS Production and Apoptosis in Prostate Cancer Cells.Toxins · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relationship between T-2 toxin and deoxynivalenol (DON) and the risk of Kashin-Beck disease is still controversial since it is poorly known about their selectivity in cartilage damage. We aimed to compare the cytotoxicity of T-2 toxin and DON on cell lines representative of cell types encountered in vivo, including human chondrocytes (C28/I2), human hepatic epithelial cells (L-02) and human tubular epithelial cells (HK-2). In addition, we determined the distribution of T-2 toxin and DON in Sprague-Dawley (SD) rats after a single dose exposure. T-2 toxin or DON decreased proliferation in a time- and concentration-dependent manner and their combination showed a similar antagonistic effect in C28/I2, L-02 and HK-2 cells. Moreover, we observed cell cycle arrest and apoptosis, associated with increased oxidative stress and decline in mitochondrial membrane potential induced by T-2 toxin and/or DON. In vivo study showed that T-2 toxin and DON did not accumulate preferentially in the knee joint compared to liver and kidney after an acute exposure in SD rats. These results suggest that T-2 toxin and/or DON inhibit proliferation and induce apoptosis through a possible mechanism involving reactive oxygen species-mediated mitochondrial pathway that is not specific for chondrocytes in vitro or joint tissues in vivo.
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Registered trials
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