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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Authors | Jiangtao Liu, Linlin Wang, Xiong Guo, Qingjiang Pang, Shixun Wu, Cuiyan Wu, Peng Xu, Yidong Bai |
Journal | PloS one
(PLoS One)
Vol. 9
Issue 9
Pg. e108394
( 2014)
ISSN: 1932-6203 [Electronic] United States |
PMID | 25264878
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antioxidants
- Reactive Oxygen Species
- Cytochromes c
- Electron Transport Complex IV
- Citrate (si)-Synthase
- Caspase 3
- Caspase 9
- Electron Transport Complex III
- Glutathione
- Selenium
- T-2 Toxin
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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
(metabolism)
- 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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