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The absorption, metabolism and excretion of 3-acetyldeoxynivalenol (3-aDON) in pigs were studied. Pigs with a faecal microflora known to be able to de-epoxidate trichothecenes were used in the experiment. The pigs were fed a commercial diet with 3-aDON added in a concentration of 2.5 mg/kg feed for 2.5 days. No traces of 3-aDON or its de-epoxide metabolite were found in plasma, urine or faeces. Deoxynivalenol (DON) was detected in plasma as soon as 20 min after start of the feeding. The maximum concentration of DON in plasma was reached after 3 h and decreased rapidly thereafter. Only low concentrations close to the detection limit were found in plasma 8 h after start of the feeding. A significant part of the DON in plasma was in a glucuronide-conjugated form (42 +/- 7%). No accumulation of DON occurred in plasma during the 60 h of exposure. The excretion of DON was mainly in urine (45 +/- 26% of the toxin ingested by the pigs) and only low amounts of metabolites of 3-aDON (2 +/- 0.4%) were recovered in faeces. De-epoxide DON constituted 52 +/- 15% of the total amount of 3-aDON-metabolites detected in faeces. The remaining part in faeces was DON. DON was still present in the urine and faeces at the end of the sampling period 48 h after the last exposure. The results show that no de-epoxides are found in plasma or urine in pigs after trichothecene exposure, even in pigs having a faecal microflora with a de-epoxidation activity. The acetylated form of the toxin is deacetylated in vivo. Furthermore, the experiment shows that the main part of DON is rapidly excreted and does not accumulate in plasma, but a minor part of the toxin is retained and slowly excreted from the pigs.

The capacity of pig gastrointestinal microflora to metabolise the trichothecenes 3-acetyl-deoxynivalenol (3-acDON) and nivalenol (NIV) was investigated. 3-acDON was deacetylated to DON in anaerobic incubations with pig faeces collected at different pig farms. Furthermore, both 3-acDON and NIV were metabolised to the corresponding deepoxy metabolite in these incubates. Five pigs, in which the gastrointestinal microflora lacked the ability to transform 3-acDON and NIV to their corresponding de-epoxidated metabolites, were given low levels of DON in the feed for seven weeks. The gastrointestinal micro-organisms did not acquire the de-epoxidation ability during the seven week long exposure period. At the end of the exposure period, faeces from pigs with a known de-epoxidation ability was spread out in the pens and left for 24 hours. One week after the faeces had been spread out in the pens, the de-epoxidation ability was found in faecal incubations from four out of five experimental pigs. This change in metabolic ability of the intestinal de-epoxidation ability was not accompanied by any detectable changes in the DNA-profiles of the bacterial community composition. The results show that the intestinal de-epoxidation ability is common at pig farms in the Uppsala area, and that the ability may be transferred between pigs in a stock.

Moulded and mycotoxin containing barley was incorporated into the diets for laying hens to study the effects on performance and health. Health indicators were different blood plasma parameters and liver vitamin A and E levels. A total of 30 hens were fed 3 diets, one supplemented with 30% of toxin-free and two with differently moulded barley from 1997 and 1998 for 7 weeks. The moulded diets contained low to moderate concentrations of ochratoxin A, zearalenone, deoxynivalenol and nivalenol. Inclusion of mouldy barley in the diets had an adverse effect on feed intake, feed conversion, digestibility of nutrients, egg production and egg quality. Plasma alkaline phosphatase was increased and certain biochemical blood parameters (bilirubin, uric acid, chlorine, protein, albumin, vitamin A) were also higher or changed compared to control. The ochratoxin A contamination although relatively low could have contributed to some of these effects as well as reduced intake of feed. The higher mould contamination and an unidentified cell-toxic constituent in the diet containing barley from 1998 can probably also explain the more marked effects from this diet.

Changes in the activity of enzymes involved in oxidative metabolism of glutamine, and in protein content, in the epithelial tissue along the gastrointestinal (GI) tract of growing pigs exposed to nivalenol (NIV) in the diet were investigated. The epithelial tissue was taken from the stomach, small intestine and colon of three groups of animals fed diets without NIV (control), with inclusion of 2.5 mg NIV/kg diet (low dose) and with inclusion of 5.0 mg NIV/kg diet (high dose). The activities of glutaminase, glutamate dehydrogenase, oxoglutarate dehydrogenase, isocitrate dehydrogenase and alanine aminotransferase were determined. In the control pigs the activities of oxoglutarate dehydrogenase and alanine aminotransferase were higher (P < 0.05) in the epithelium of the small intestine as compared with the stomach and colon, while there were no differences in the activities of glutaminase, glutamate dehydrogenase and isocitrate dehydrogenase. With increasing inclusion of NIV in the diet the activity of oxoglutarate dehydrogenase decreased (P < 0.05) in the epithelium of the small intestine and colon, and the activity of alanine aminotransferase tended (P = 0.07) to increase in the epithelium of the small intestine. The activities of glutaminase, glutamate dehydrogenase and isocitrate dehydrogenase remained unaffected by the inclusion of NIV in the diet. In the control pigs the protein content in the epithelium of the small intestine was higher (P < 0.05) than in the stomach and colon, while there were no effects of NIV inclusion in the diet on the protein content. It can be concluded from the present study that the epithelial tissue of the small intestine and colon of pigs exposed to a diet containing NIV will have a reduced enzymatic capacity to utilise alpha-ketoglutarate in the tricarboxylic acid cycle (TCA-cycle), suggesting an impaired energy supply to these organs.

The absorption and metabolism of nivalenol (NIV) were studied in pigs fed 0.05 mg NIV/kg BW, twice daily. Blood samples were taken during the first and third day, through catheters in the hepatic portal vein and peripheral mesenteric artery. Nivalenol was detected in most of the earliest blood samples, taken twenty minutes after the start of feeding. During 7.5 hrs after feeding, 11-43% of the NIV dose was absorbed. The systemic peak concentrations were 3-6 ng NIV/ml, mostly occurring 2.5-4.5 h after feeding. Sixteen hours after feeding, NIV was still being absorbed from the intestine, and the systemic concentrations were 1-3 ng NIV/ml. Nivalenol was mainly excreted in faeces, which contained concentrations up to 3.2 mg NIV/kg. No metabolites of NIV were found in plasma, urine, and faeces, either as glucuronic acid or sulphate conjugates, or as de-epoxy-NIV, indicating a lack of metabolism. The feeding of NIV did not cause feed refusal, and measured clinical plasma parameters were within the normal ranges.