Taranu Ionelia, Braicu Cornelia, Marin Daniela Eliza, Pistol Gina Cecilia, Motiu Monica, Balacescu Loredana, Beridan Neagoe Ioana, Burlacu Radu
Laboratory of Animal Biology, National Institute for Research and Development for Biology and Animal Nutrition, Calea Bucuresti No. 1, Balotesti, Ilfov 077015, Romania.
National Institute for Research and Development for Oncology "Prof. Dr. Ion Chiricuta", Str. Republicii, No. 34-36, Cluj-Napoca, Romania.
Toxicol Lett. 2015 Jan 5;232(1):310-25. doi: 10.1016/j.toxlet.2014.10.022. Epub 2014 Oct 23.
The gut represents the main route of intoxication with mycotoxins. To evaluate the effect and the underlying molecular changes that occurred when the intestine is exposed to zearalenone, a Fusarium sp mycotoxin, porcine epithelial cells (IPEC-1) were treated with 10μM of ZEA for 24h and analysed by microarray using Gene Spring GX v.11.5. Our results showed that 10μM of ZEA did not affect cell viability, but can increase the expression of toll like receptors (TLR1-10) and of certain cytokines involved in inflammation (TNF-α, IL-1β, IL-6, IL-8, MCP-1, IL-12p40, CCL20) or responsible for the recruitment of immune cells (IL-10, IL-18). Microarray results identified 190 genes significantly and differentially expressed, of which 70% were up-regulated. ZEA determined the over expression of ITGB5 gene, essential against the attachment and adhesion of ETEC to porcine jejunal cells and of TFF2 implicated in mucosal protection. An up-regulation of glutathione peroxidase enzymes (GPx6, GPx2, GPx1) was also observed. Upon ZEA challenge, genes like GTF3C4 responsible for the recruitment of polymerase III and initiation of tRNA transcription in eukaryotes and STAT5B were significantly higher induced. The up-regulation of CD97 gene and the down-regulation of tumour suppressor genes (DKK-1, PCDH11X and TC531386) demonstrates the carcinogenic potential of ZEA.
肠道是霉菌毒素中毒的主要途径。为了评估肠道暴露于玉米赤霉烯酮（一种镰刀菌属霉菌毒素）时所产生的影响及潜在的分子变化，用10μM玉米赤霉烯酮处理猪上皮细胞（IPEC - 1）24小时，并使用Gene Spring GX v.11.5通过微阵列进行分析。我们的结果表明，10μM的玉米赤霉烯酮不影响细胞活力，但可增加 toll 样受体（TLR1 - 10）以及某些参与炎症的细胞因子（TNF-α、IL - 1β、IL - 6、IL - 8、MCP - 1、IL - 12p40、CCL20）或负责免疫细胞募集的细胞因子（IL - 10、IL - 18）的表达。微阵列结果鉴定出190个显著差异表达的基因，其中70%上调。玉米赤霉烯酮导致ITGB5基因过表达，该基因对肠毒素大肠杆菌附着和黏附于猪空肠细胞至关重要，还导致参与黏膜保护的TFF2过表达。还观察到谷胱甘肽过氧化物酶（GPx6、GPx2、GPx1）上调。在玉米赤霉烯酮刺激后，负责真核生物中聚合酶III募集和tRNA转录起始的GTF3C4基因以及STAT5B基因的诱导显著增加。CD97基因的上调和肿瘤抑制基因（DKK - 1、PCDH11X和TC531386）的下调表明玉米赤霉烯酮具有致癌潜力。
