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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Main Authors: Yang Lei, Zhao Guanghui, Wang Xi, Wang Yingting, Lin Xialu, Yu Fangfang, Mary B. Goldring, Guo Xiong, Mikko J. Lammi
Format: Article
Language:English
Published: Nature Portfolio 2017-05-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-017-02568-5
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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
collection DOAJ
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.
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spelling doaj.art-0aff6a293be84ac8831c3ff2090268942022-12-21T23:38:24ZengNature PortfolioScientific Reports2045-23222017-05-017111410.1038/s41598-017-02568-5Cellular responses to T-2 toxin and/or deoxynivalenol that induce cartilage damage are not specific to chondrocytesYang Lei0Zhao Guanghui1Wang Xi2Wang Yingting3Lin Xialu4Yu Fangfang5Mary B. Goldring6Guo Xiong7Mikko J. Lammi8School of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionHong Hui Hospital, Health Science Center, Xi’an Jiaotong UniversitySchool of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionSchool of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionSchool of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionSchool of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionHospital for Special Surgery, Weill Cornell Medical CollegeSchool of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionSchool of Public Health, Health Science Center, Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning CommissionAbstract 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.https://doi.org/10.1038/s41598-017-02568-5
spellingShingle 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
Scientific Reports
title 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_short 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
url https://doi.org/10.1038/s41598-017-02568-5
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