Deoxynivalenol, also known as vomitoxin, is a foodborne mycotoxin, acting as a potent inhibitor of protein synthesis. It stimulates the pro-inflammatory response, causes ribotoxic stress, cytotoxicity and apoptosis, as well as results in the impairment of multiple physiological functions, such as the intestinal barrier, growth, immune regulation and reproduction [1].?
In immortalized human kidney epithelial cells, deoxynivalenol induced cytotoxicity, with EC50 value of 1.1 μM [2]. In cloned macrophages and monocytes, the Jurkat human T-cell model, and cloned B cells, deoxynivalenol triggered apoptosis at concentrations ranging from 100 to 1000 ng/ml [3].?
In swine, 50 μg/kg deoxynivalenol (i.p. or oral) could elicit emesis. Rapid onset of vomiting in pigs also occurred upon ingestion of feed contaminated with 19.7 ppm deoxynivalenol. Swine consuming 2 and 4 ppm deoxynivalenol exhibited a dose-related decrease in weight gain within the first 8 weeks of feeding, with 4 ppm causing decreased feed intake, weight gain, and efficiency of feed utilization throughout the experiment [3].?
References:
[1]. Vidal A, Claeys L, Mengelers M, et al. Humans significantly metabolize and excrete the mycotoxin deoxynivalenol and its modified form deoxynivalenol-3-glucoside within 24 hours. Scientific Reports, 2018, 8(1): 5255.
[2]. Bretz M, Beyer M, Cramer B, et al. Thermal degradation of the Fusarium mycotoxin deoxynivalenol. Journal of Agricultural and Food Chemistry, 2006, 54(17): 6445-6451.
[3]. Pestka J J. Deoxynivalenol: mechanisms of action, human exposure, and toxicological relevance. Archives of Toxicology, 2010, 84(9): 663-679.
