Deoxynivalenol in the Gastrointestinal Tract of Immature Gilts under per os Toxin Application

Abstract

Deoxynivalenol is also known as vomitoxin due to its impact on livestock through interference with animal growth and acceptance of feed. At the molecular level, deoxynivalenol 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. Because of concerns related to deoxynivalenol, the United States FDA has instituted advisory levels of 5 µg/g for grain products for most animal feeds and 10 µg/g for grain products for cattle feed. The aim of the study was to determine the effect of low doses of deoxynivalenol applied per os on the presence of this mycotoxin in selected tissues of the alimentary canal of gilts. The study was performed on 39 animals divided into two groups (control, C; n = 21 and experimental, E; n = 18), of 20 kg body weight at the beginning of the experiment. Gilts received the toxin in doses of 12 µg/kg b.w./day (experimental group) or placebo (control group) over a period of 42 days. Three animals from two experimental groups were sacrificed on days 1, 7, 14, 21, 28, 35 and 42, excluding day 1 when only three control group animals were scarified. Tissues samples were prepared for high performance liquid chromatography (HPLC) analyses with the application of solid phase extraction (SPE). The results show that deoxynivalenol doses used in our study, even when applied for a short period, resulted in its presence in gastrointestinal tissues. The highest concentrations of deoxynivalenol reported in small intestine samples ranged from 7.2 (in the duodenum) to 18.6 ng/g (in the ileum) and in large intestine samples from 1.8 (in transverse the colon) to 23.0 ng/g (in the caecum). In liver tissues, the deoxynivalenol contents ranged from 6.7 to 8.8 ng/g.

The genotoxicity of caecal water from gilts following experimentally induced Fusarium mycotoxicosis

“…The most significant increase in genotoxicity was observed after the sixth week of the experiment in the distal colon, which was probably caused by the accumulation of ZEN, DON, and ZEN + DON in porcine tissues. In our previous study (Waskiewicz et al 2014) it was shown that DON, even when applied for a short period, resulted in its presence in gastrointestinal tissues. The concentrations of DON reported in the large intestine samples increased gradually from the second (in the proximal part) and from the fourth (in the distal part) week of experiment, and ranged from 2.5 to 20.52 ng/g (in ascending colon) and from 6.75 to 20.0 ng/g (in descending colon).…”

“…It seems possible that differences in the feed form could modulate the bioavailability of DON, as it could affect the liberation of the toxin from the matrix and thereby influence residue concentration in the animal tissue. In this study, the daily DON intake during the whole period of the experiment reflects slight differences between animals because of DON doses converted into body weight and precisely administered by a small portion of the feed matrix (Waskiewicz et al 2014). …”

The effects of dietary deoxynivalenol (DON) on selected blood biochemical and hematological parameters in pre-pubertal gilts

“…The vena cava cranialis is situated remotely from the liver (detoxification) and the kidneys (excretion), organs that are directly adjacent to the gastrointestinal system. The results of hematological profiles during exposure to low doses of DON and at relatively low carry-over factor of DON to the intestines (towards the end of the experiment) and the liver (highest values were found in week 1) (Waśkiewicz et al 2014) led to minor, but statistically significant changes in the values of selected indicators. The first changes were observed in weeks 2 and 3 in biochemical indices, such as AlAT (Fig.…”

“…The bioavailability of DON can differ in various forms of feed, which can affect the release of the analyzed mycotoxin from the matrix and its retention in animal tissues. A study of samples collected from the same pre-pubertal gilts (Waśkiewicz et al 2014) demonstrated that the degree of tissue accumulation (liver and intestinal sections) of DON is determined not only by the dose, but also by the duration of exposure. The longer the exposure period, the higher the accumulation levels of DON in the examined tissues, which ultimately supported the determination of the carry-over factor (Völkel et al 2011) after different exposure times.…”

“…Through the epoxide group, DON can bind with a high number of eukaryotic ribosomal subunits and disrupt the activity of peptide transferase, thus disrupting the elongation or shortening of peptide chains. Due to its ability to impair protein synthesis, DON can affect the rate of cellular transport, enzyme metabolism in the cytoplasm and changes in affinity for the active binding site (Waśkiewicz et al 2014). For this reason, DON affects specific tissues and organs.…”