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Open AccessArticle

Cytotoxic Properties of HT-2 Toxin in Human Chondrocytes: Could T3 Inhibit Toxicity of HT-2?

1
School of Public Health, Health Science Center of Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health Commission of the People’s Republic of China, Xi’an 710061, China
2
Department of Integrative Medical Biology, University of Umeå, 90187 Umeå, Sweden
*
Authors to whom correspondence should be addressed.
Toxins 2019, 11(11), 667; https://doi.org/10.3390/toxins11110667
Received: 27 September 2019 / Revised: 5 November 2019 / Accepted: 9 November 2019 / Published: 15 November 2019
(This article belongs to the Special Issue Mycotoxin Exposure and Related Diseases)
Thyroid hormone triiodothyronine (T3) plays an important role in coordinated endochondral ossification and hypertrophic differentiation of the growth plate, while aberrant thyroid hormone function appears to be related to skeletal malformations, osteoarthritis, and Kashin-Beck disease. The T-2 toxin, present extensively in cereal grains, and one of its main metabolites, HT-2 toxin, are hypothesized to be potential factors associated with hypertrophic chondrocyte-related osteochondropathy, known as the Kashin-Beck disease. In this study, we investigated the effects of T3 and HT-2 toxin on human chondrocytes. The immortalized human chondrocyte cell line, C-28/I2, was cultured in four different groups: controls, and cultures with T3, T3 plus HT-2 and HT-2 alone. Cytotoxicity was assessed using an MTT assay after 24-h-exposure. Quantitative RT-PCR was used to detect gene expression levels of collagen types II and X, aggrecan and runx2, and the differences in runx2 were confirmed with immunoblot analysis. T3 was only slightly cytotoxic, in contrast to the significant, dose-dependent cytotoxicity of HT-2 alone at concentrations ≥ 50 nM. T3, together with HT-2, significantly rescued the cytotoxic effect of HT-2. HT-2 induced significant increases in aggrecan and runx2 gene expression, while the hypertrophic differentiation marker, type X collagen, remained unchanged. Thus, T3 protected against HT-2 induced cytotoxicity, and HT-2 was an inducer of the pre-hypertrophic state of the chondrocytes. View Full-Text
Keywords: triiodothyronine; HT-2 toxin; cytotoxicity; Kashin-Beck disease triiodothyronine; HT-2 toxin; cytotoxicity; Kashin-Beck disease
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Zhang, F.; Lammi, M.J.; Shao, W.; Zhang, P.; Zhang, Y.; Wei, H.; Guo, X. Cytotoxic Properties of HT-2 Toxin in Human Chondrocytes: Could T3 Inhibit Toxicity of HT-2? Toxins 2019, 11, 667.

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