Abstract
The relationship between T-2 toxin and deoxynivalenol (DON) and the risk of Kashin-Beck disease is still controversial since it is poorly known about their selectivity in cartilage damage. We aimed to compare the cytotoxicity of T-2 toxin and DON on cell lines representative of cell types encountered in vivo, including human chondrocytes (C28/I2), human hepatic epithelial cells (L-02) and human tubular epithelial cells (HK-2). In addition, we determined the distribution of T-2 toxin and DON in Sprague-Dawley (SD) rats after a single dose exposure. T-2 toxin or DON decreased proliferation in a time- and concentration-dependent manner and their combination showed a similar antagonistic effect in C28/I2, L-02 and HK-2 cells. Moreover, we observed cell cycle arrest and apoptosis, associated with increased oxidative stress and decline in mitochondrial membrane potential induced by T-2 toxin and/or DON. In vivo study showed that T-2 toxin and DON did not accumulate preferentially in the knee joint compared to liver and kidney after an acute exposure in SD rats. These results suggest that T-2 toxin and/or DON inhibit proliferation and induce apoptosis through a possible mechanism involving reactive oxygen species-mediated mitochondrial pathway that is not specific for chondrocytes in vitro or joint tissues in vivo.
Highlights
The trichothecenes are a large group of secondary metabolites mainly produced by the fungi of Fusarium genus[1]
Contamination of food by mycotoxins, especially T-2 toxin and DON have been widely considered as risk factor for Kashin-Beck disease (KBD) mainly based on extensive epidemiological studies, which showed that cereal or food samples analyzed from KBD areas were more heavily contaminated with these toxins compared to those in non-KBD areas[23,24,25,26,27,28]
According to the IC50 values, T-2 toxin was less cytotoxic on C28/I2 and HK-2 cells than on L-02 cells, and DON was less cytotoxic on C28/I2 cells than on L-02 and HK-2 cells (Table 1)
Summary
The trichothecenes are a large group of secondary metabolites mainly produced by the fungi of Fusarium genus[1]. The T-2 toxin and deoxynivalenol (DON), belonging to type A and type B trichothecenes, are highly toxic and the most common mycotoxins because of their widespread dissemination[1] Both T-2 toxin and DON promote the generation of cellular reactive oxygen species (ROS), which can further induce lipid peroxidation, DNA damage, and cell apoptosis in different cell types[6, 7]. Due to their co-occurrence in nature, the combined toxic effects of these mycotoxin mixtures have received more consideration[8,9,10,11,12]. To verify if mycotoxins could accumulate in joint tissues, we examined their tissue distribution in knee joint, liver and kidney of Sprague-Dawley (SD) rats after acute oral administration of T-2 toxin and DON
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