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Deoxynivalenol induces apoptosis in mouse thymic epithelial cells through mitochondria-mediated pathway

Authors
Journal
Environmental Toxicology and Pharmacology
1382-6689
Publisher
Elsevier
Volume
38
Issue
1
Identifiers
DOI: 10.1016/j.etap.2014.05.015
Keywords
  • Deoxynivalenol
  • Mtec1 Cells
  • P53
  • Apoptosis
  • Ros
  • Mitochondrial
Disciplines
  • Biology

Abstract

Abstract Deoxynivalenol (DON) is a mycotoxin produced as a secondary metabolite by fungal species. In this report, we investigated the apoptotic effect of DON in mouse thymic epithelial cell line 1 (MTEC1). MTEC1 cell apoptosis induced by DON was confirmed by nuclei morphology change, TUNEL positive staining, annexin V/propidium iodide positive staining and increased protein levels of caspase-3, caspase-8, caspase-9 and poly(ADP-ribose) polymerase (PARP). The effects of DON on reactive oxygen species (ROS) levels and mitochondrial membrane potential were investigated via fluorescence microscope and flow cytometry, respectively. In addition, DON could significantly increase the protein levels of p53 and Bax/Bcl-2 ratio in MTEC1 cells. Taken together, our results suggest that DON causes the activation of p53, increased levels of ROS and the induction of mitochondrial dysfunction, which may contribute to DON-induced apoptosis in MTEC1 cells.

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