Deoxynivalenol: Mechanisms of action and its effects on various terrestrial and aquatic species.

Deoxynivalenol, a type B trichothecene mycotoxin produced by Fusarium species of fungi, is a ubiquitious contaminant of cereal grains worldwide. Chronic, low dose consumption of feeds contaminated with DON is associated with a wide range of symptoms in terrestrial and aquatic species including decreased feed intake and feed refusal, reduced weight gain, and altered nutritional efficiency. Acute, high dose exposure to DON may be associated with more severe symptoms such as vomiting, diarrhea, intestinal inflammation and gastrointestinal hemorrhage. The toxicity of DON is partly related to its ability to disrupt eukaryotic protein synthesis via binding to the peptidyl transferase site of the ribosome. Moreover, DON exerts its effects at the cellular level by activating mitogen activated protein kinases (MAPK) through a process known as the ribotoxic stress response (RSR). The outcome of DON-associated MAPK activation is dose and duration dependent; acute low dose exposure results in immunostimulation characterized by the upregulation of cytokines, chemokines and other proinflammatory-related proteins, whereas longer term exposure to higher doses generally results in apoptosis, cell cycle arrest, and immunosuppression. The order of decreasing sensitivity to DON is considered to be: swine > rats > mice > poultry ≈ ruminants. However, studies conducted within the past 10 years have demonstrated that some species of fish, such as rainbow trout, are highly sensitive to DON. The aims of this review are to explore the effects of DON on terrestrial and aquatic species as well as its mechanisms of action, metabolism, and interaction with other Fusarium mycotoxins. Notably, a considerable emphasis is placed on reviewing the effects of DON on different species of fish.