Trichothecene mycotoxins are a group of structurally similar fungal metabolites that are capable of producing a wide range of toxic effects. Deoxynivalenol (DON, vomitoxin), a trichothecene, is prevalent worldwide in crops used for food and feed production, including in Canada and the United States. Although DON is one of the least acutely toxic trichothecenes, it should be treated as an important food safety issue because it is a very common contaminant of grain. This review focuses on the ability of DON to induce toxicologic and immunotoxic effects in a variety of cell systems and animal species. At the cellular level, the main toxic effect is inhibition of protein synthesis via binding to the ribosome. In animals, moderate to low ingestion of toxin can cause a number of as yet poorly defined effects associated with reduced performance and immune function. The main overt effect at low dietary concentrations appears to be a reduction in food consumption (anorexia), while higher doses induce vomiting (emesis). DON is known to alter brain neurochemicals. The serotoninergic system appears to play a role in mediation of the feeding behavior and emetic response. Animals fed low to moderate doses are able to recover from initial weight losses, while higher doses induce more long-term changes in feeding behavior. At low dosages of DON, hematological, clinical, and immunological changes are also transitory and decrease as compensatory/adaptation mechanisms are established. Swine are more sensitive to DON than mice, poultry, and ruminants, in part because of differences in metabolism of DON, with males being more sensitive than females. The capacity of DON to alter normal immune function has been of particular interest. There is extensive evidence that DON can be immunosuppressive or immunostimulatory, depending upon the dose and duration of exposure. While immunosuppression can be explained by the inhibition of translation, immunostimulation can be related to interference with normal regulatory mechanisms. In vivo, DON suppresses normal immune response to pathogens and simultaneously induces autoimmune-like effects which are similar to human immunoglobulin A (IgA) nephropathy. Other effects include superinduction of cytokine production by T helper cells (in vitro) and activation of macrophages and T cells to produce a proinflammatory cytokine wave that is analogous to that found in lipopolysaccharide-induced shock (in vivo). To what extent the elevation of cytokines contributes to metabolic effects such as decreased feed intake remains to be established. Although these effects have been largely characterized in the mouse, several investigations with DON suggest that immunotoxic effects are also likely in domestic animals. Further toxicology studies and an assessment of the potential of DON to be an etiologic agent in human disease are warranted.

Toxicology of deoxynivalenol (vomitoxin).

The trichothecene mycotoxin deoxynivalenol (DON) is produced in wheat, barley and corn following infestation by the fungus Fusarium in the field and during storage. Colloquially known as “vomitoxin” because of its emetic effects in pigs, DON has been associated with human gastroenteritis. Since DON is commonly detected in cereal foods, there are significant questions regarding the risks of acute poisoning and chronic effects posed to persons ingesting this trichothecene. A further challenge is how to best manage perceived risks without rendering critical food staples unavailable to an ever-expanding world population. In experimental animal models, acute DON poisoning causes emesis, whereas chronic low-dose exposure elicits anorexia, growth retardation, immunotoxicity as well as impaired reproduction and development resulting from maternal toxicity. Pathophysiologic effects associated with DON include altered neuroendocrine signaling, proinflammatory gene induction, disruption of the growth hormone axis, and altered gut integrity. At the cellular level, DON induces ribotoxic stress thereby disrupting macromolecule synthesis, cell signaling, differentiation, proliferation, and death. There is a need to better understand the mechanistic linkages between these early dose-dependent molecular effects and relevant pathological sequelae. Epidemiological studies are needed to determine if relationships exist between consumption of high DON levels and incidence of both gastroenteritis and potential chronic diseases. From the perspective of human health translation, a particularly exciting development is the availability of biomarkers of exposure (e.g. DON glucuronide) and effect (e.g. IGF1) now make it possible to study the relationship between DON consumption and growth retardation in susceptible human populations such as children and vegetarians. Ultimately, a fusion of basic and translational research is needed to validate or refine existing risk assessments and regulatory standards for this common mycotoxin.

Deoxynivalenol: mechanisms of action, human exposure, and toxicological relevance.

Deoxynivalenol (DON) is a mycotoxin that commonly contaminates cereal-based foods worldwide. At the molecular level, DON disrupts normal cell function by inhibiting protein synthesis via binding to the ribosome and by activating critical cellular kinases involved in signal transduction related to proliferation, differentiation, and apoptosis. Relative to toxicity, there are marked species differences, with the pig being most sensitive to DON, followed by rodent > dog > cat > poultry > ruminants. The physiologic parameter that is most sensitive to low-level DON exposure is the emetic response, with as little as 0.05 to 0.1 mg/kg body weight (bw) inducing vomiting in swine and dogs. Chinese epidemiological studies suggest that DON may also produce emetic effects in humans. With respect to chronic effects, growth (anorexia and decreased nutritional efficiency), immune function, (enhancement and suppression), and reproduction (reduced litter size) are also adversely affected by DON in animals, whereas incidence of neoplasia is not affected. When hazard evaluations were conducted using existing chronic toxicity data and standard safety factors employed for anthropogenic additives/contaminants in foods, tolerable daily intakes (TDIs) ranging from 1 to 5 microg/kg bw have been generated. Given that critical data gaps still exist regarding the potential health effects of DON, additional research is needed to improve capacity for assessing adverse health effects of this mycotoxin. Critical areas for future DON research include molecular mechanisms underlying toxicity, sensitivity of human cells/tissues relative to other species, emetic effects in primates, epidemiological association with gastroenteritis and chronic disease in humans, and surveillance in cereal crops worldwide.

Deoxynivalenol: Toxicology and Potential Effects on Humans

Deoxynivalenol: Toxicity, mechanisms and animal health risks

Mycotoxins are toxic and carcinogenic metabolites produced by fungi that colonize food crops. The most agriculturally important mycotoxins known today are aflatoxins, which cause liver cancer and have also been implicated in child growth impairment and acute toxicoses; fumonisins, which have been associated with esophageal cancer (EC) and neural tube defects (NTDs); deoxynivalenol (DON) and other trichothecenes, which are immunotoxic and cause gastroenteritis; and ochratoxin A (OTA), which has been associated with renal diseases. This review describes the adverse human health impacts associated with these major groups of mycotoxins. First, we provide background on the fungi that produce these different mycotoxins and on the food crops commonly infected. Then, we describe each group of mycotoxins in greater detail, as well as the adverse effects associated with each mycotoxin and the populations worldwide at risk. We conclude with a brief discussion on estimations of global burden of disease caused by dietary mycotoxin exposure.

Public Health Impacts of Foodborne Mycotoxins

Summary Four trials were conducted with young pigs to evaluate the effect of dietary level of vomitoxin-contaminated corn on performance and pathology. A dietary level of approximately 20 ppm vomitoxin caused vomiting, 12 ppm vomitoxin caused almost complete feed refusal and 1.3 ppm caused a significant depression in feed intake and rate of gain. No lesions attributable to vomitoxin were observed in pigs fed up to 43 ppm dietary vomitoxin for a 21-d period. Alterations in various blood serum characteristics were observed in pigs fed vomitoxin, however, the effects could not be separated from those that may result from low intake of food.

Vomitoxin in corn fed to young pigs.

Thirty barrows (average weight 8.4 kg) were used in a 3-wk experiment to determine the effects of the ingestion of vomitoxin (deoxynivalenol)-contaminated feed on performance and blood chemistry. The barrows were assigned randomly to consume either: 1) a control diet (C), fed ad libitum, 2) a vomitoxin contaminated diet (V; 10.5 ppm), fed ad libitum, or 3) a vomitoxin contaminated pair-fed at levels equal to those consumed by V animals (PF). The V and PF pigs had similar daily gains (.19 vs .20 kg) and feed intakes (.40 and .39 kg), but both of these were lower (P less than .01) than those for the C-fed pigs (.38 kg daily gain and .72 kg feed intake). The V-fed pigs had lower (P less than .05) hematocrit, hemoglobin, serum glucose and serum phosphorus and tended to have lower serum calcium (P less than .06) than C-fed pigs. The V-fed pigs had higher (P less than .05) hemoglobin and tended to have higher (P less than .08) serum phosphorus and lower (P less than .07) serum calcium than PF animals. There was a high total- and free-bilirubin concentration in serum of C- and V-fed pigs in the last sampling period (3-wk), which may be due to fasting and not cholestasis. No differences among treatments were observed in any of the other blood parameters. These results suggest that the differences in animal performance and blood parameters observed between control-and vomitoxin-fed pigs are mainly due to differences in feed intake.

The Effects of Vomitoxin and Feed Intake on the Performance and Blood Characteristics of Young Pigs

Vitamin E Stability in Corn and Mixed Feed

Ninety pigs approximately 5 weeks of age were used in an investigation of the influence of three levels of supplemental selenium (0, .60 and 1.20 ppm), and three levels of supplemental vitamin E (0, 60, 120 ppm) in a factorial arrangement, on reproduction. The pigs were confined to 18 pens with three gilts and two boars per pen. \"/'he basal diet was formulated using high moisture ensiled corn, which was later changed to high moisture propionic acid treated corn, and soybean meal supplemented with minerals and vitamins excluding selenium and vitamin E. The basal dict contained .03 gtg/g selenium and .35 pg/g ~-tocopherol on a dry matter basis. The assigned diets were fed throughout the experiment. Nine of the 10 pigs fed the basal dict died by day 57 of the experiment with lesions observed in seven of these pigs suggesting mulberry hcart disease, and/or hepatosis dietetica and/or gastric ulcers. The reason for the death of two of the piglets was not determined. One pig fed the highest level of selenium and no supplemental vitamin E died on day 23 of the experiment. No other pigs died during the experiment and no lesions of vitamin E-selenium deficiency were observed in pigs which were killed. There was no obvious influence of supplemented selenium or vitamin E on reproductive performance of surviving gilts, bowcver, the number of gilts per treatment was small. Supplementation of gilt diets with selenium or vitamin E resulted in increased levels of the nutrients in their serum and colostrum as well as in their baby pigs' serum. There was a greater

Selenium and Vitamin E Supplementation of High Moisture Corn Diets for Swine Reproduction

Influence of Method of Corn Storage and Vitamin E and Selenium Supplementation on Pig Survival and Reproduction

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