Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes

Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes

Blog Article

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 USE OF AUTHENTIC FILMS WITH SUBTITLES IN THE PROCESS OF LEARNING NEW VOCABULARY IN HIGHER EDUCATION SECTOR (AS BASED ON THE ENGLISH LANGUAGE MATERIAL) 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 Influence of Prolonged Salting on the Physicochemical Properties of Duck Egg White 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.