Transcriptome Analysis of Caco-2 Cells upon the Exposure of Mycotoxin Deoxynivalenol and Its Acetylated Derivatives
Key Laboratory for Deep Processing of Major Grain and Oil of Ministry of Education, Wuhan Polytechnic University, Wuhan 430023, China
China National Center for Food Safety Risk Assessment, NHC Key Laboratory of Food Safety Risk Assessment, Food Safety Research Unit (2019RU014) of Chinese Academy of Medical Science, Beijing 100000, China
Author to whom correspondence should be addressed.
Toxins 2021, 13(2), 167; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13020167
Received: 7 January 2021 / Revised: 16 February 2021 / Accepted: 19 February 2021 / Published: 22 February 2021
(This article belongs to the Section Mycotoxins)
Deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-ADON) and 15-acetyldeoxynivalenol (15-ADON) are type B trichothecenes; one of the major pollutants in food and feed products. Although the toxicity of DON has been well documented, information on the toxicity of its acetylated derivative remains incomplete. To acquire more detailed insight into 3-ADON and 15-ADON, Caco-2 cells under 0.5 µM DON, 3-ADON and 15-ADON treatment for 24 h were subjected to RNA-seq analysis. In the present study, 2656, 3132 and 2425 differentially expressed genes (DEGs) were selected, respectively, and were enriched utilizing the Kyoto Encyclopedia of Genes and Genomes (KEGG) and the Gene Ontology (GO) database. The upregulation of ataxia-telangiectasia mutated kinase (ATM), WEE1 homolog 2 (WEE2) and downregulation of proliferating cell nuclear antigen (PCNA), minichromosome maintenance (MCMs), cyclin dependent kinase (CDKs), and E2Fs indicate that the three toxins induced DNA damage, inhibition of DNA replication and cell cycle arrest in Caco-2 cells. Additionally, the upregulation of sestrin (SENEs) and NEIL1 implied that the reason for DNA damage may be attributable to oxidative stress. Our study provides insight into the toxic mechanism of 3-ADON and 15-ADON.