Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytesVisa övriga samt affilieringar
2017 (Engelska)Ingår i: Scientific Reports, E-ISSN 2045-2322, Vol. 7, nr 1, s. 2231-
Artikel i tidskrift (Refereegranskat) Published
Abstract [en]
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.
Ort, förlag, år, upplaga, sidor
London: Nature Publishing Group, 2017. Vol. 7, nr 1, s. 2231-
Nyckelord [en]
Kashin-Beck disease, T-2 toxin, deoxynivalenol, chondrocyte
Nationell ämneskategori
Ortopedi Farmakologi och toxikologi Cell- och molekylärbiologi
Forskningsämne
cellforskning; medicinsk cellbiologi; patologi; toxikologi
Identifikatorer
URN: urn:nbn:se:umu:diva-135354DOI: 10.1038/s41598-017-02568-5ISI: 000401754200018PubMedID: 28533525Scopus ID: 2-s2.0-85019699780OAI: oai:DiVA.org:umu-135354DiVA, id: diva2:1098377
2017-05-242017-05-242023-03-23Bibliografiskt granskad