Abstract
Deoxynivalenol (DON) is a type B trichothecene mycotoxin that is commonly detected in cereals and grains world-wide. The low-tolerated levels of this mycotoxin, especially in mono-gastric animals, reflect its bio-potency. The toxicity of DON is conventionally attributed to its ability to inhibit ribosomal protein biosynthesis, but recent advances in molecular tools have elucidated novel mechanisms that further explain DON’s toxicological profile, complementing the diverse symptoms associated with its exposure. This article summarizes the recent findings related to novel mechanisms of DON toxicity as well as how structural modifications to DON alter its potency. In addition, it explores feasible ways of expanding our understating of DON-cellular targets and their roles in DON toxicity, clearance, and detoxification through the utilization of computational biology approaches.
Highlights
Type B trichothecene mycotoxins are common contaminants of grains and cereals around the world.The presence of these fungal secondary-metabolites raises public-health concerns at both the agriculture and food industry levels
In the southern region of Brazil, DON was detected within the 243–2281 μg/kg range in almost half (47%) of whole wheat grain samples collected during the 2012 crop season [3]
Due to the complex toxicological profile of DON and its sporadic occurrence, it is suggested that the current tolerated limits of DON in human food and animal feed do not provide sufficient protection from the associated risks of DON exposure [4]. In this mini-review we summarize the recent findings related to the mechanism(s) of DON toxicity as well as how structural modifications to DON alter its potency
Summary
Type B trichothecene mycotoxins are common contaminants of grains and cereals around the world The presence of these fungal secondary-metabolites raises public-health concerns at both the agriculture and food industry levels. Due to the complex toxicological profile of DON and its sporadic occurrence, it is suggested that the current tolerated limits of DON in human food and animal feed do not provide sufficient protection from the associated risks of DON exposure [4]. In this mini-review we summarize the recent findings related to the mechanism(s) of DON toxicity as well as how structural modifications to DON alter its potency. We shed light on how such knowledge can practically aid in understanding DON toxicity and identifying possible routes of detoxification in nature
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