title: Deoxynivalenol induces apoptosis in mouse thymic epithelial cells through mitochondria-mediated pathway.
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.
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Daotong
authors: D
authors: Li
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Haoran
authors: H
authors: Ma
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Yaqiong
authors: Y
authors: Ye
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Changyun
authors: C
authors: Ji
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Xiaohong
authors: X
authors: Tang
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Dan
authors: D
authors: Ouyang
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Jian
authors: J
authors: Chen
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
authors: Yugu
authors: Y
authors: Li
authors: College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China. Electronic address: mayongjiang@scau.edu.cn.
authors: Yongjiang
authors: Y
authors: Ma
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D020169:Caspases / Q000378:metabolism; D002460:Cell Line; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology; D014255:Trichothecenes / Q000633:toxicity*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D014255:Trichothecenes; D016159:Tumor Suppressor Protein p53; D011065:Poly(ADP-ribose) Polymerases; D020169:Caspases; C007262:deoxynivalenol
keywords: Apoptosis; Deoxynivalenol; MTEC1 cells; Mitochondrial; P53; ROS