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The role of mitochondria in T-2 toxin-induced human chondrocytes apoptosis.

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.
AuthorsJiangtao Liu, Linlin Wang, Xiong Guo, Qingjiang Pang, Shixun Wu, Cuiyan Wu, Peng Xu, Yidong Bai
JournalPloS one (PLoS One) Vol. 9 Issue 9 Pg. e108394 ( 2014) ISSN: 1932-6203 [Electronic] United States
PMID25264878 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antioxidants
  • Reactive Oxygen Species
  • Cytochromes c
  • Electron Transport Complex III
  • Electron Transport Complex IV
  • Citrate (si)-Synthase
  • Caspase 3
  • Caspase 9
  • Glutathione
  • Selenium
  • T-2 Toxin
Topics
  • Antioxidants (metabolism)
  • Apoptosis (immunology)
  • Cartilage, Articular (cytology)
  • Caspase 3 (metabolism)
  • Caspase 9 (metabolism)
  • Cell Survival (drug effects)
  • Chondrocytes (immunology)
  • Citrate (si)-Synthase (metabolism)
  • Cytochromes c (secretion)
  • Electron Transport Complex III (metabolism)
  • Electron Transport Complex IV (metabolism)
  • Enzyme Activation
  • Fusarium (pathogenicity)
  • Glutathione (metabolism)
  • Humans
  • Kashin-Beck Disease (immunology, pathology)
  • Middle Aged
  • Mitochondria (immunology, pathology)
  • Reactive Oxygen Species (metabolism)
  • Selenium (pharmacology)
  • T-2 Toxin (antagonists & inhibitors, immunology, pharmacology)

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