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Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes.
School of Public Health, Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Xi'an, P.R. China.
Hong Hui Hospital, Health Science Center, Xi'an Jiaotong University, Xi'an, P.R. China.
School of Public Health, Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Xi'an, P.R. China.
School of Public Health, Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Xi'an, P.R. China.
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2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, no 1, 2231- p.Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
London: Nature Publishing Group, 2017. Vol. 7, no 1, 2231- p.
Keyword [en]
Kashin-Beck disease, T-2 toxin, deoxynivalenol, chondrocyte
National Category
Orthopedics Pharmacology and Toxicology Cell and Molecular Biology
Research subject
cellforskning; Medical Cell Biology; Pathology; Toxicology
Identifiers
URN: urn:nbn:se:umu:diva-135354DOI: 10.1038/s41598-017-02568-5PubMedID: 28533525OAI: oai:DiVA.org:umu-135354DiVA: diva2:1098377
Available from: 2017-05-24 Created: 2017-05-24 Last updated: 2017-05-24

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