Vomitoxin

Vomitoxin, also known as deoxymivalenol is a type B trichothecene, an epoxy-sesquiterpenoid. It occurs mostly in grains such as wheat, barley, oats, rye and maize. It is produced in grain infected by Fusarium head blight. It is not a know carcinogen, so grain with vomitoxin would have to be ingested in very high amounts to pose as a health risk to humans. However it can affect flavors in food and processing performance. Human food products are restricted to a 1 ppm level established by the FDA. The FDA advisory levels are: || || || || || Similarly, vomitoxin (right) is a toxin that's produced by certain types of fungus that grow on wheat and barley. Its proper name is deoxynivalenol, but was given the trivial name vomitoxin because it caused vomiting in pigs that had eaten contaminated wheat. Vomitoxin is a known carcinogen and when mixed with grains in high amounts, it can be a risk to humans. When compared to other mycotoxins it is relatively mild.
 * 1 ppm || Finished wheat products, such as flour, bran and germ, that potentially may be consumed by humans. The FDA does not set an advisory level for raw grain intended for milling because normal manufacturing practices and additional technology available to millers can substantially reduce DON levels in the finished wheat product. However, individual millers or food industries may have stricter requirements than 1 ppm. ||
 * 10 ppm || Grains and byproducts destined for ruminating beef and feedlot cattle older than 4 months and for poultry, providing that these ingredients don't exceed 50 percent of the diet ||
 * 5 ppm || Grains and grain byproducts destined for swine, providing that these ingredients don't exceed 20 percent of the diet ||
 * 5 ppm || Grains and grain byproducts destined for all other animals, providing that these ingredients don't exceed 40 percent of the diet ||

Vomitoxin (VT) and other trichothecene mycotoxins mediate a broad range of immunotoxic effects via the induction of inflammation-associated genes in leukocytes. The purpose of this study was to test the hypothesis that VT induces cyclooxygenase-2 (COX-2) gene expression in macrophages and that this is regulated at the level of mitogen-activated protein kinases (MAPKs). Exposure of the murine macrophage cell line RAW 264.7 to 50–250 ng/ml VT for 24 h markedly enhanced the production of prostaglandin E2 (PGE2), a major COX-2 metabolite. PGE2 elevation was preceded by increases in COX-2 mRNA (2 h) and COX-2 protein (15 h) in VT-treated cells. VT induced rapid (15 min) and persistent (up to 240 min) phosphorylation of extracellular, signal regulated protein kinases 1 and 2 (ERK1/2) and p38 MAPK as well as a rapid (15 min) but transient (up to 60 min) phosphorylation of c-Jun N-terminal kinases 1 and 2 (JNK1/2). The ERK inhibitor PD98059 and p38 inhibitor SB203580 suppressed VT-induced PGE2 and COX-2 protein expression, whereas impairment of JNK function by transient transfection with a dominant negative (dn) JNK vector had no effect on COX-2 protein expression. Relatedly, in cells transfected with a COX-2 promoter-luciferase construct, PD98059- and SB203580-, but not dnJNK-treatment, suppressed VT-induced luciferase transcription. VT also increased COX-2 mRNA stability, and this was inhibited by PD98059 but not by SB203580. Taken together, these results indicate that VT-induced PGE2 production and COX-2 expression by elevating transcriptional activity and mRNA stability. Enhanced transcriptional activity was modulated by ERK and p38 signaling pathways, whereas mRNA stability was promoted exclusively by VT-activated p38 phosphorylation. These data provide insight into possible general mechanisms by which VT and other trichlothecenes upregulate proinflammatory genes and impart immunotoxicity.

//F. graminearum// grows optimally at a temperature of 25°C and at a water activity above 0.88. //F. culmorum// grows optimally at 21°C and at a water activity above 0.87. The geographical distribution of the two species appears to be related to temperature, //F. graminearum// being the more common species occurring in warmer climates. Deoxynivalenol has been implicated in incidents of mycotoxicoses in both humans and farm animals. **__ Seen everyday in: __**


 * Human foods: Vomitoxin is not a known carcinogen as with aflatoxin. Large amounts of grain with vomitoxin would have to be consumed to pose a health risk to humans. The U.S. Food and Drug Administration has established a level of 1 ppm (parts per million) restriction of vomitoxin.
 * Companion animals: Dogs and cats are restricted to 5 ppm and of grains and grain byproducts and the grains are not to exceed 40% percent of the diet.
 * Livestock and farm animals: In animals and livestock, vomitoxin causes a refusal to feed and lack of weight gain when fed above advised levels. Restrictions are set at 10 ppm for poultry and ruminating beef and feedlot cattle older than four months. Ingredients may not exceed 50% of the animal's diet. Dairy cow feed limits are set at 2 ppm.

__Toxicity:__
When compared to other trichothecene mycotoxins which can form in grains and forages, vomitoxin is relatively mild. Reduced feed intake, with its accompanying decrease in performance, is the only symptom of vomitoxin toxicity livestock producers will likely encounter. This response to vomitoxin appears to occur through the central nervous system. Vomitoxin belongs to a class of mycotoxins (tricothecenes) which are strong inhibitors of protein synthesis; exposure to vomitoxin causes the brain to increase its uptake of the amino acid tryptophan and, in turn, its synthesis of serotonin. Increased levels of serotonin are believed to be responsible for the anorexic effects of DON and other tricothecenes. Irritation of the gastrointestinal tract may also play a role in reducing feed intake, and may also partially explain the high incidence of paraesophageal stomach ulcers observed in sows during feed refusal.