Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

Toxicol Lett. 2018 Mar 1;284:213-221. doi: 10.1016/j.toxlet.2017.11.035. Epub 2017 Dec 1.


Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 μM; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cellular respiration significantly altered. Molecular functions linked to mitochondrial respiratory chain and oxidoreductase activity were over-represented (q-value < 0.01). Pathway analysis revealed oxidative phosphorylation and electron transport chain as the most significantly altered pathways in all studied doses (z-score > 1.96; adj p-value < 0.05). 77 genes involved in the respiratory chain were significantly down-regulated at least at one dose. Moreover, 21 genes related to apoptosis and programmed cell death, and 12 genes related to caspase activity were significantly altered, mainly affecting initiator caspases 8, 9 and 10. The results demonstrated BEA-induced mitochondrial damage affecting the respiratory chain, and pointing to apoptosis through the caspase cascade in human lymphoblastic T cells.

Keywords: Beauvericin; Immunotoxicology; Jurkat; RNA-seq; Toxicogenomics; Transcriptomics.

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Cell Culture Techniques
  • Cell Membrane Permeability / drug effects
  • Cell Membrane Permeability / genetics
  • Depsipeptides / toxicity*
  • Dose-Response Relationship, Drug
  • Electron Transport
  • Gene Expression Profiling
  • Gene Ontology
  • Humans
  • Jurkat Cells
  • Oxidative Phosphorylation
  • Oxidative Stress / drug effects*
  • Oxidative Stress / genetics
  • Transcriptome / drug effects*


  • Depsipeptides
  • beauvericin