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

Jiangtao Liu, Linlin Wang, Xiong Guo, Qingjiang Pang, Shixun Wu, Cuiyan Wu, Peng Xu, Yidong Bai

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42 Scopus citations


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 timedependent 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.

Original languageEnglish (US)
Article numbere108394
JournalPloS one
Issue number9
StatePublished - 2014

ASJC Scopus subject areas

  • General


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