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

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 e...

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Autores principales:	Yang Lei, Zhao Guanghui, Wang Xi, Wang Yingting, Lin Xialu, Yu Fangfang, Mary B. Goldring, Guo Xiong, Mikko J. Lammi
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/0aff6a293be84ac8831c3ff209026894
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spelling	oai:doaj.org-article:0aff6a293be84ac8831c3ff2090268942021-12-02T15:05:56ZCellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes10.1038/s41598-017-02568-52045-2322https://doaj.org/article/0aff6a293be84ac8831c3ff2090268942017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02568-5https://doaj.org/toc/2045-2322Abstract 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.Yang LeiZhao GuanghuiWang XiWang YingtingLin XialuYu FangfangMary B. GoldringGuo XiongMikko J. LammiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yang Lei Zhao Guanghui Wang Xi Wang Yingting Lin Xialu Yu Fangfang Mary B. Goldring Guo Xiong Mikko J. Lammi Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
description	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.
format	article
author	Yang Lei Zhao Guanghui Wang Xi Wang Yingting Lin Xialu Yu Fangfang Mary B. Goldring Guo Xiong Mikko J. Lammi
author_facet	Yang Lei Zhao Guanghui Wang Xi Wang Yingting Lin Xialu Yu Fangfang Mary B. Goldring Guo Xiong Mikko J. Lammi
author_sort	Yang Lei
title	Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
title_short	Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
title_full	Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
title_fullStr	Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
title_full_unstemmed	Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
title_sort	cellular responses to t-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/0aff6a293be84ac8831c3ff209026894
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Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytes

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