Literature DB >> 31863870

Comparison of the toxic mechanism of T-2 toxin and deoxynivalenol on human chondrocytes by microarray and bioinformatics analysis.

Lei Yang1, Suiqin Wang2, Guanghui Zhao3, Xi Wang4, Xiong Guo5.   

Abstract

T-2 toxin and deoxynivalenol (DON) are two representative mycotoxins that are commonly found in cereals and agricultural products. As T-2 toxin and DON are considered the cause of Kashin-Beck disease, a special osteoarticular disease, chondrocytes would be a vital target site for these toxins. To fully understand the toxicity effects of T-2 toxin and DON on chondrocytes, the present study investigated and compared the gene expression profiles and underlying mechanisms of T-2 toxin and DON on cultured human chondrocytes by microarray and bioinformatics analysis. Normal human chondrocytes were treated with T-2 toxin at 0.01 μg/ml and DON at 1.0 μg/ml for 72 h and analyzed by microarray using Affymetrix Human Gene Chip. Comprehensive analysis, including gene ontology, pathways and gene-gene networks was performed to identify the crucial gene functions, related signal pathways and key genes. A total of 175 and 237 differentially expressed genes were identified in human chondrocytes for T-2 toxin and DON treatment, respectively. Of these, 47 had the same expression tendencies in the two groups. The protein-protein interaction network analysis showed that the 10 hub genes were different between the two groups. Our results provide a comprehensive understanding of the toxic mechanism of T-2 toxin and DON on human chondrocytes and suggest that although T-2 toxin and DON showed some similar toxic mechanisms in human chondrocytes, they also had different toxic characteristics.
Copyright © 2019 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Bioinformatics analysis; Chondrocytes; Deoxynivalenol; Gene expression; T-2 toxin

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Year:  2019        PMID: 31863870     DOI: 10.1016/j.toxlet.2019.12.024

Source DB:  PubMed          Journal:  Toxicol Lett        ISSN: 0378-4274            Impact factor:   4.372


  3 in total

1.  Thyroid Hormone Metabolite 3-Iodothyronamine (T1AM) Alleviates Hypoxia/Reoxygenation-Induced Cardiac Myocyte Apoptosis via Akt/FoxO1 Pathway.

Authors:  Haiyan Zhou; Bailong Hu; Xingde Liu
Journal:  Med Sci Monit       Date:  2020-03-12

2.  Comparative Transcriptome Analysis Reveals the Potential Cardiovascular Protective Targets of the Thyroid Hormone Metabolite 3-Iodothyronamine (3-T1AM).

Authors:  Zhou Haiyan; Hu Bailong; Zhang Bei; Wang Yiming; Liu Xingde
Journal:  Biomed Res Int       Date:  2020-06-19       Impact factor: 3.411

3.  Cellobiose inhibits the release of deoxynivalenol from transformed deoxynivalenol-3-glucoside from Lactiplantibacillus plantarum.

Authors:  Kailin Li; Lan Wang; Dianzhen Yu; Zheng Yan; Na Liu; Aibo Wu
Journal:  Food Chem (Oxf)       Date:  2022-01-20
  3 in total

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