Current sights for mechanisms of deoxynivalenol‐induced hepatotoxicity and prospective views for future scientific research: A mini review

• Published in: Journal of applied toxicology Vol. 37; no. 5; pp. 518 - 529
• Main Authors: Peng, Zhao, Chen, Liangkai, Nüssler, Andreas K., Liu, Liegang, Yang, Wei
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.05.2017
• Subjects: Animals; apoptosis; Cereals; Chemical and Drug Induced Liver Injury - pathology; DON; hepatic toxicity; Humans; Liver; Liver - metabolism; Liver - pathology; liver damage; molecule pathways; Mycotoxins - pharmacokinetics; Mycotoxins - toxicity; Pathology; Toxicity; Trichothecenes - pharmacokinetics; Trichothecenes - toxicity; apoptosis; DON; molecule pathways; liver damage; hepatic toxicity
• ISSN: 0260-437X; 1099-1263
• DOI: 10.1002/jat.3428

Deoxynivalenol (DON) belongs to the group B trichothecenes, which are the most common mycotoxins in cereal commodities. It is very stable within the temperature range 170–350 °C, showing no reduction in its concentration after 30 min at 170 °C. This chemical property is a very dangerous factor for human and animal health. Liver is also responsible for the detoxification and formation of DON‐glucuronide in both human and animals. Some studies already demonstrated that DON could induce liver damage remarkably through DON altering expressions of p53, caspase‐3, caspase‐7, caspase‐8 and Bax in different cell lines. At the same time, other publications illustrated some opposite results. At present, a full and systematic discussion of the hepatic toxicity of DON is still lacking. Therefore, the aim of the present review is to summarize and update the prominent evidence, regarding DON effects on liver tissues and cell lines. Moreover, based on the current studies we outline some of the identified molecule targets or pathways involved in DON‐induced hepatotoxicity, and put forward our opinions and suggest an hypothesis for future research. Copyright © 2016 John Wiley & Sons, Ltd. In this table, we have shown that DON induced liver damage with positive and negative results in different animal models and cell lines. This mycotoxin can evokes obvious pathological changes in tissue by altering repssions of relative enzymes or oxidative stress. Otherwise, DON can induces expressions of apoptotic proteins thereby producing hepatic fibrosis and other kinds of liver damage.