ArticlePloS one2014
The role of mitochondria in T-2 toxin-induced human chondrocytes apoptosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 76 citations in OpenAlex.
- Impacts of trichothecene mycotoxins on human colonic epithelial cells: molecular mechanisms and signaling pathways.Journal of advanced research · 2026Review
- Magnetofection-mediated siRNA delivery ameliorates cartilage damage in Kashin-Beck diseaseTheranostics · 2026Article
- Transcriptomics and Metabolomics Insights into the Dysregulation of Chondrocyte Differentiation Induced by T-2 Toxin.International journal of molecular sciences · 2025Article
- Integrative Proteome and Transcriptome Analyses Reveal the Metabolic Disturbance of the Articular Cartilage in Kashin-Beck Disease, an Endemic Arthritis.International journal of molecular sciences · 2025Article
- Ellagic Acid Reduces Cadmium Exposure-Induced Apoptosis in HT22 Cells via Inhibiting Oxidative Stress and Mitochondrial Dysfunction and Activating Nrf2/HO-1 Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging.Aging and disease · 2024Review
- Comparative Analysis of Gut Microbiota from Rats Induced by Se Deficiency and T-2 Toxin.Nutrients · 2023Article
- DNA Damage Induced by T-2 Mycotoxin in Human Skin Fibroblast Cell Line-Hs68.International journal of molecular sciences · 2023Article
- Selenomethionine Antagonized microRNAs Involved in Apoptosis of Rat Articular Cartilage Induced by T-2 Toxin.Toxins · 2023Article
- Mitochondrial Damage Induced by T-2 Mycotoxin on Human Skin-Fibroblast Hs68 Cell Line.Molecules (Basel, Switzerland) · 2023Article
- Article
- The molecular mechanism study of COMP involved in the articular cartilage damage of Kashin-Beck disease.Bone & joint research · 2020Article
- Article
- Beneficial Effects of Rosmarinic Acid on IPEC-J2 Cells Exposed to the Combination of Deoxynivalenol and T-2 Toxin.Mediators of inflammation · 2020Article
- Article
- Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes.Scientific reports · 2017Article
- Exposure to HT-2 toxin causes oxidative stress induced apoptosis/autophagy in porcine oocytes.Scientific reports · 2016Article
- Copper, iron, and selenium dietary deficiencies negatively impact skeletal integrity: A review.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- The effects of T-2 toxin on the prevalence and development of Kashin-Beck disease in China: a meta-analysis and systematic review.Toxicology research · 2016Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-2 toxin, a mycotoxin produced by Fusarium species, has been shown to cause diverse toxic effects in animals and is also a possible pathogenic factor of Kashin-Beck disease (KBD). The role of mitochondria in KBD is recognized in our recent research. The aim of this study was to evaluate the role of mitochondria in T-2 toxin-induced human chondrocytes apoptosis to understand the pathogenesis of KBD. T-2 toxin decreased chondrocytes viabilities in concentration- and time-dependent manners. Exposure to T-2 toxin can reduce activities of mitochondrial complexes III, IV and V, ΔΨm and the cellular ATP, while intracellular ROS increased following treatment with T-2 toxin. Furthermore, mitochondrial cytochrome c release, caspase-9 and 3 activation and chondrocytes apoptosis were also obviously observed. Interestingly, Selenium (Se) can partly block T-2 toxin -induced mitochondria dysfunction, oxidative damage and chondrocytes apoptosis. These results suggest that the effect of T-2 toxin on human chondrocytes apoptosis may be mediated by a mitochondrial pathway, which is highly consistent with the chondrocytes changes in KBD.
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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.