Ochratoxin A-Induced Apoptosis of IPEC-J2 Cells through ROS-Mediated Mitochondrial Permeability Transition Pore Opening Pathway.
Hong WangYing ChenNianhui ZhaiXingxiang ChenFang GanHu LiKehe HuangPublished in: Journal of agricultural and food chemistry (2017)
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 mitochondrial 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.
Keyphrases
- induced apoptosis
- oxidative stress
- diabetic rats
- endoplasmic reticulum stress
- cell death
- reactive oxygen species
- cell cycle arrest
- dna damage
- high glucose
- signaling pathway
- endothelial cells
- drug induced
- high throughput
- single cell
- south africa
- cell proliferation
- drug delivery
- stem cells
- bone marrow
- combination therapy
- cancer therapy
- stress induced