Journal
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 65, Issue 48, Pages 10630-10637Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.7b04434
Keywords
Ochratoxin A; IPEC-J2 cells; mitochondrial reactive oxygen species; mitochondrial permeability transition pore opening; apoptosis
Funding
- National Key RD Program [2016YFD0501203]
- National Natural Science Foundation of China [31472253]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (Jiangsu, China)
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With the purpose to explore the mechanisms associated with the intestinal toxicity of Ochratoxin A (OTA), an intestinal porcine epithelial cell line (IPEC-J2) was applied in this study as in vitro models for intestinal epithelium. The results confirmed that OTA induced IPEC-J2 cell toxicity by MTT assay and apoptosis by Hoechst 33258 staining and flow cytometer analysis. We also observed that OTA induced the mitochondria! reactive oxygen species (ROS) production and mitochondrial permeability transition pore (mPTP) opening by confocal microscopy. Western blot showed that OTA induced cytochrome c (cyt-c) release and caspase-3 activation, which could be suppressed by inhibition of mPTP opening with cyclosporin A. Treatment with Mito-TEMPO, the mitochondria-targeted ROS scavenger, blocked OTA-induced mitochondrial ROS generation and mPTP opening and prevented cyt-c release, caspase-3 activation, and apoptosis in IPEC-J2 cells.
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