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.
Highlights
T-2 toxin is a highly toxic trichothecene mycotoxin, and a naturally occurring mold byproduct of Fusarium species which is toxic to humans and animals [1]
It was indicated that the dysfunction of the mitochondria play an important role in Kashin–Beck disease (KBD) chondrocyte damages in our recent study, and T-2 toxin, a possible pathogenic factor of KBD, increases Bax protein production and induces chondrocyte apoptosis [19,20,23,24]
The present data from analyses of cell viability, mitochondrial function and mitochondria- mediated apoptosis reveal that T-2 toxin caused insults to human chondrocytes via a mitochondrial pathway
Summary
T-2 toxin is a highly toxic trichothecene mycotoxin, and a naturally occurring mold byproduct of Fusarium species which is toxic to humans and animals [1]. Dietary ingestion represents the most common route of human exposure. It is detected in a number of field crops (wheat, maize, barley and oats) and processed grains (malt, beer and bread) [2,3]. Trichothecenes are recognized as having multiple inhibitory effects on eukaryote cells, including inhibition of protein, DNA and RNA synthesis, inhibition of mitochondria electron transport system, mitochondrial function, and mitochondrial protein synthesis, effects on cell division and membrane effects [4]. T-2 toxin induced apoptosis has been considered to be one of the important mechanisms in its toxic effects [6]
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