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Ochratoxin A-Induced Apoptosis of IPEC-J2 Cells through ROS-Mediated Mitochondrial Permeability Transition Pore

Hong Wang1, Ying Chen1, Nianhui Zhai1

  • 1College of Veterinary Medicine, and ‡Institute of Nutritional and Metabolic Disorders in Domestic Animals and Fowls, Nanjing Agricultural University , Nanjing, Jiangsu Province 210095, China.

Journal of Agricultural and Food Chemistry
|November 15, 2017
PubMed

Insights

Ochratoxin A (OTA) triggers intestinal cell damage by increasing oxidative stress and mitochondrial dysfunction. Inhibiting reactive oxygen species (ROS) or mitochondrial pores protects intestinal cells from OTA toxicity.

Area of Science:

  • Toxicology
  • Cell Biology
  • Biochemistry

Background:

  • Ochratoxin A (OTA) is a common food contaminant with known toxicity.
  • Understanding OTA's impact on intestinal epithelium is crucial for public health.
  • Intestinal porcine epithelial cells (IPEC-J2) serve as a relevant in vitro model.

Purpose of the Study:

  • To elucidate the mechanisms underlying Ochratoxin A (OTA)-induced intestinal toxicity.
  • To investigate the role of mitochondrial dysfunction and oxidative stress in OTA toxicity.
  • To evaluate potential protective strategies against OTA-induced intestinal damage.

Main Methods:

  • Utilized IPEC-J2 cell line as an in vitro model for intestinal epithelium.
  • Assessed cell viability using MTT assay.
  • Detected apoptosis via Hoechst 33258 staining and flow cytometry.
  • Measured mitochondrial reactive oxygen species (ROS) production and mitochondrial permeability transition pore (mPTP) opening using confocal microscopy.
  • Analyzed cytochrome c (cyt-c) release and caspase-3 activation by Western blot.
  • Investigated the effects of cyclosporin A (mPTP inhibitor) and Mito-TEMPO (ROS scavenger).

Main Results:

  • OTA significantly induced IPEC-J2 cell toxicity and apoptosis.
  • OTA exposure led to increased mitochondrial ROS generation and mPTP opening.
  • Western blot confirmed OTA-induced cytochrome c release and caspase-3 activation.
  • Cyclosporin A and Mito-TEMPO treatments effectively suppressed OTA-induced mitochondrial dysfunction and apoptosis.
  • Mito-TEMPO blocked ROS generation, mPTP opening, and subsequent apoptotic events.

Conclusions:

  • OTA induces intestinal cell toxicity primarily through mitochondrial oxidative stress and mPTP opening.
  • Mitochondrial ROS generation is a key event in the OTA-induced apoptotic pathway.
  • Targeting mitochondrial ROS and mPTP opening presents a viable strategy to mitigate OTA-induced intestinal damage.
Keywords:
IPEC-J2 cellsOchratoxin Aapoptosismitochondrial permeability transition pore openingmitochondrial reactive oxygen species

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