The samples were fixed in 4% buffered formalin for 48 h

The samples were fixed in 4% buffered formalin for 48 h. area in both DON treated groups. The absolute or relative organ weights (liver, heart, proventriculus, gizzard, small intestine, spleen, pancreas, colon, cecum, bursa of Fabricius and thymus) were not altered (P> 0.05) in broilers fed the diet containing DON compared with controls. DON and de-epoxy-DON (DOM-1) were analyzed in serum, bile, liver, feces and digesta from consecutive segments of the digestive tract (gizzard, cecum, and Lanopepden rectum). Concentrations of DON and its metabolite DOM-1 in serum, bile, and liver were lower than the detection limits of the applied liquid chromatography coupled with mass spectrometry (LC-MS/MS) method. Only about 10 to 12% and 6% of the ingested DON was recovered in gizzard and feces, irrespective of the dietary DON-concentration. However, the DON recovery in the EP cecum as percentage of DON-intake varied between 18 to 22% and was not influenced by dietary DON-concentration. Interestingly, in the present trial, DOM-1 did not appear in the large intestine and in feces. The results indicate that deepoxydation in the present study hardly occurred in the distal segments of the digestive tract, assuming that the complete de-epoxydation occurs in the proximal small intestine where the majority of the parent toxin is absorbed. In conclusion, diets with DON contamination below levels that induce a negative impact on performance could alter small intestinal morphology in broilers. Additionally, the results confirm that the majority of the ingested DON quickly disappears through the gastrointestinal tract. Keywords:broiler,Fusariummycotoxin, deoxynivalenol, small intestine, morphology, metabolism == 1. Introduction == The mycotoxin deoxynivalenol (DON), the most prevalent trichothecene mycotoxin contaminating crops in Europe and North America [1], is commonly detected in cereals and grains. DON is a public health concern, as it is resistant to milling, processing and heating and readily enters the food chain. The digestive tract is a target for DON. The gastrointestinal mucosa serves as a dynamic barrier regulating uptake of nutrients and water, while excluding potential pathogens and toxicants [2]. Following ingestion of contaminated food or feed, intestinal Lanopepden epithelial cells could be exposed to a high concentration of toxicants, potentially affecting intestinal functions [3]. All animal species tested have been shown to be susceptible to DON. However, the degree of susceptibility varies according to the following order: pigs > mice > rats > poultry ruminants [4]. The difference in sensitivity may be explained by differences in absorption, distribution, metabolism, and elimination of DON [5]. In general, poultry are less sensitive to DON compared to other species [6,7]. Negative effects on the performance of broilers occurred in dietary concentrations greater Lanopepden than 5 ppm, but in some investigations [8,9] even higher concentrations did not consistently induce clinical signs. One important aspect of DON toxicity is an injury of the gastrointestinal tract. Although it is a food and feed contaminant, only scarce reports exist on the gastrointestinal effects of DON [1014]. Critical gaps still exist regarding the potential effects of DON, and widespread animal exposure needs additional research to improve capacity for assessing adverse effects of DON. Understanding the effects of DON on the gastrointestinal tract is of major importance for protecting animal health and risk assessment. Preluskyet Lanopepden al. [4] reported some changes in pigs fed a diet containing low levels of DON, including alterations Lanopepden in stomach and serum proteins, and suggesting specific effects ofFusariumtoxins and particularly DON. The injury of the gastrointestinal tract, involving thickening of the mucosa of the stomach and a higher degree of folding, is one important characteristic of DON toxicity [15]. In addition, Awadet al. [12] found that feeding of broilers with DON artificially contaminated diets at 10.