The toxicity mechanisms of DON to humans and animals and potential biological treatment strategies

Crit Rev Food Sci Nutr. 2023;63(6):790-812. doi: 10.1080/10408398.2021.1954598. Epub 2021 Sep 14.

Abstract

Deoxynivalenol, also known as vomitotoxin, is produced by Fusarium, belonging to the group B of the trichothecene family. DON is widely polluted, mainly polluting cereal crops such as wheat, barley, oats, corn and related cereal products, which are closely related to lives of people and animals. At present, there have been articles summarizing DON induced toxicity, biological detoxification and the protective effect of natural products, but there is no systematic summary of this information. In addition to ribosome and endoplasmic reticulum, recent investigations support that mitochondrion is also organelles that DON can damage. DON can't directly act on mitochondria, but can indirectly cause mitochondrial damage and changes through other means. DON can indirectly inhibit mitochondrial biogenesis and mitochondrial electron transport chain activity, ATP production, and mitochondrial transcription and translation. This review will provide the latest progress on mitochondria as the research object, and systematically summarizes all the toxic mechanisms of DON. Here, we discuss DON induced mitochondrial-mediated apoptosis and various mitochondrial toxicity. For the toxicity of DON, many methods have been derived to prevent or reduce the toxicity. Biological detoxification and the antioxidant effect of natural products are potentially effective treatments for DON toxicity.

Keywords: Deoxynivalenol; antioxidant; biological detoxification; toxicity mechanism.

Publication types

  • Review

MeSH terms

  • Animals
  • Antioxidants / pharmacology
  • Crops, Agricultural*
  • Edible Grain*
  • Humans
  • Mitochondria
  • Triticum

Substances

  • Antioxidants