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.
Toxins (Basel). 2021 Feb 22;13(2):167. doi: 10.3390/toxins13020167.
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.
脱氧雪腐镰刀菌烯醇（DON）、3-乙酰脱氧雪腐镰刀菌烯醇（3-ADON）和 15-乙酰脱氧雪腐镰刀菌烯醇（15-ADON）是 B 型单端孢霉烯族化合物，是食品和饲料产品中的主要污染物之一。尽管 DON 的毒性已得到充分证实，但关于其乙酰化衍生物毒性的信息仍不完整。为了更详细地了解 3-ADON 和 15-ADON，本研究用 0.5µM DON、3-ADON 和 15-ADON 处理 Caco-2 细胞 24 小时，进行 RNA-seq 分析。在本研究中，分别选择了 2656、3132 和 2425 个差异表达基因（DEGs），并利用京都基因与基因组百科全书（KEGG）和基因本体论（GO）数据库进行了富集分析。结果表明，ATM、WEE2 的上调和 PCNA、MCMs、CDKs 和 E2Fs 的下调表明，这三种毒素诱导了 Caco-2 细胞中的 DNA 损伤、DNA 复制抑制和细胞周期停滞。此外，SENEs 和 NEIL1 的上调表明，DNA 损伤的原因可能归因于氧化应激。本研究为 3-ADON 和 15-ADON 的毒性机制提供了新的见解。
