In two feeding trials the effect of nivalenol (NIV) on male broiler chickens was studied. A commercial starter diet was provided for ad libitum consumption throughout the whole experiment. The NIV was added to the feed when the birds were 7 d old. Growth and feed consumption were thereafter registered every 5th d during 20 d. In the first trial birds were offered feed containing 0, .5, 2.5, or 5 ppm NIV. The only variable that significantly differed from the control was the concentration of uric acid in plasma, which was increased by 94 and 66%, respectively, in treatment groups 2.5 and 5 ppm. In the second trial, NIV-concentrations of 0, 3, 6, and 12 ppm were used. The weight gain for the 20-d period was decreased by 11% with 6 and 12 ppm. During this period these birds showed a decrease of about 6% in feed consumption and feed conversion efficiency. Gizzard erosions were found in 33% of the birds fed 12 ppm NIV and in 8% of those fed 3 or 6 ppm. No such erosions were found in the control birds. Relatively, the liver weights in the 12 ppm group were reduced more than total body weights. No effects on relative organ weights were found when bursa, spleen, and gizzard were compared to control. In the blood, no change compared to control was found in hematocrit or in the plasma concentration of glucose, calcium, cholesterol, triglycerides, and uric acid, or in the plasma activity of aspartate amino transferase, alanine amino transferase, or gamma glutamyl transpeptidase.

The capacity of the gastrointestinal microflora of pig, cow, and chicken to metabolize nivalenol (NIV) and deoxynivalenol (DON) was studied both in vivo and in vitro. Before feeding NIV to pigs, no metabolites of NIV or DON were formed in anaerobic incubates of the toxins with the pigs feces. However, after one week on a diet containing 2.5 or 5 ppm NIV, nearly all excreted NIV in feces had been de-epoxidated in five of six pigs. After three weeks on the NIV diet also the sixth pig had acquired this ability. Deoxynivalenol was also de-epoxidated when incubated in vitro with the microorganisms that formed de-epoxy-NIV in vivo. Anaerobic incubation of NIV and DON with cow rumen fluid produced de-epoxides of both toxins in a high proportion. No de-epoxide of NIV, but another unidentified metabolite was found in feces from chicken fed 2.5 or 5 ppm NIV for three weeks.

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.

Nivalenol has been analysed in Swedish cereals between 1987 and 1990 and it was found in oats (35% of all samples), barley (13%) and wheat (4%), with a high yearly variation. The highest concentration was 4700 micrograms/kg. Nivalenol-producing strains of Fusarium poae were isolated from contaminated samples. Feeding nivalenol to chicks produced no toxic effects at concentrations below 5 mg/kg and only small effects at 6 and 12 mg/kg.

Young pigs were fed diets to which 0, 2.5, or 5 mg/kg of purified nivalenol (NIV) had been added. The exposure continued for 3 weeks without any signs of feed refusal, vomiting, or change in clinical appearance, and there were no changes in body or organ weights due to the exposure. However, the concluding macroscopic examination revealed gastrointestinal erosions and signs of nephropathy in most of the exposed pigs. There were no differences in total or differential blood leukocyte counts between control and exposed pigs in blood samples collected after 0, 1, or 3 weeks, nor in the number of thymocytes at the end of the trial. Spleen cell numbers showed a dose‐dependent decrease after 3 weeks of exposure that was statistically different from controls in pigs exposed to 5 mg NIV/kg. Flow cytometric analysis of lymphocytes revealed decreased numbers of both the CD4+ and the CD8+ subpopulations in the spleen at this point in time, reflecting the lower numbers of splenocytes; but no proportional changes were seen. In blood, exposure to NIV caused a transient decrease in the proportion of CD4+ cells after 1 week of exposure. Analysis of IgG and IgA in plasma showed a time‐dependent tendency of increasing plasma concentrations of IgA and decreasing concentrations of IgG in the 2.5 mg/kg group, but differences in Ig levels between experimental groups and controls were not observed at any time. No differences were seen in the mitogen‐induced proliferation by lymphocytes from blood, spleen, or thymus. In conclusion, exposure of young pigs to NIV in the diet caused pathological alterations in the kidneys and gastrointestinal tract and reduced the number of splenocytes. The results also indicated that exposure to NIV caused a time‐dependent increase in IgA production in the 2.5 mg/kg group. Nat. Toxins 5:238–246, 1997. © 1998 Wiley‐Liss, Inc.