Deoxynivalenol inhibits proliferation and induces apoptosis in human umbilical vein endothelial cells

Environ Toxicol Pharmacol. 2016 Apr:43:232-41. doi: 10.1016/j.etap.2016.02.002. Epub 2016 Mar 26.

Abstract

Deoxynivalenol (DON) is a stable mycotoxins found in cereals infected by certain fungal species and causes adverse health effects in animals and human such as vomiting, diarrhea and reproductive toxicity. In this study, we investigated the toxic and apoptotic effects of DON in human umbilical vein endothelial cells (HUVECs), a good model for studying inflammation. The results show that DON significantly inhibited the viability of HUVECs. DON could also inhibit the proliferation of HUVECs through G2/M phase arrest in cell cycle progression. Moreover, oxidative stress induced by DON was indicated by observations of increased levels of reactive oxygen species (ROS). In addition, DON also causes mitochondrial damage by decreasing the mitochondrial membrane potential and inducing apoptosis by up-regulation of apoptosis-related genes like caspase-3, caspase-9, and Bax genes, and down-regulation of Bcl-2 gene. These results together suggest that DON could induce cell cycle arrest, oxidative stress, and apoptosis in HUVECs.

Keywords: Apoptosis; Cell cycle; Deoxynivalenol; HUVECs; Mitochondrial membrane potential.

MeSH terms

  • Apoptosis
  • Caspase 3 / metabolism
  • Caspase 9 / metabolism
  • Cell Proliferation / drug effects
  • Hazardous Substances / toxicity*
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • Oxidative Stress
  • Reactive Oxygen Species / metabolism
  • Trichothecenes / toxicity*

Substances

  • Hazardous Substances
  • Reactive Oxygen Species
  • Trichothecenes
  • Caspase 3
  • Caspase 9
  • deoxynivalenol