Zearalenone induces ROS-mediated mitochondrial damage in porcine IPEC-J2 cells

J Biochem Mol Toxicol. 2017 Oct;31(10). doi: 10.1002/jbt.21944. Epub 2017 Jun 13.


In this study, the mitochondrial damage effect and mechanism of zearalenone (ZEA) in swine small intestine IPEC-J2 cells in vitro were comprehensively characterized. The analyses revealed that ZEA at high doses (8 and 7 μg/mL) can significantly increase P < 0.05 the malondialdehyde levels and decrease antioxidant enzymes activities after 48 h of exposure. Meanwhile, the reactive oxygen species (ROS) accumulation increased in high dose ZEA-treated groups after 2 h treatment, but decreased due to the ROS-induced mitochondrial damage and the caused cell apoptosis after 48 h of high does ZEA treatment. Moreover, the decreasing of mitochondrial membrane potential (MMP; ΔΨ) in high dose ZEA exposure was observed in line with the increasing ROS production in mitochondria. Results suggest that ZEA exposure can induce mitochondrial damage by reducing antioxidant enzyme activities, accumulation of ROS, and decreasing MMP. The mitochondrial damage had a dramatic concentration-effects relationship with ZEA.

Keywords: IPEC-J2 cells; antioxidant enzymes; mitochondrial damage; mitochondrial membrane potential; reactive oxygen species; zearalenone.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Cell Line
  • Intestine, Small / metabolism*
  • Intestine, Small / pathology
  • Membrane Potential, Mitochondrial / drug effects*
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Reactive Oxygen Species / metabolism*
  • Swine
  • Zearalenone / toxicity*


  • Reactive Oxygen Species
  • Zearalenone