家畜などへの影響 
As nivalenol is a mycotoxic product of certain Fusarium species it is often found in infected wheat and grain. As unprocessed wheat and grain product are often used as feed for livestock animals these are at a higher risk of nivalenol intake.

Toxicity studies in swine that received a dose of 0.05 mg nivalenol/kg body weight twice daily showed no lethal effects. Most nivalenol was secreted with the feces and did not reach the bloodstream despite the fact that there was still nivalenol upstage over the intestines after 16 hours of feeding. There were further no nivalenol metabolites found in feces or urine within the first three days. After a week of exposure to 2.5 or 5 mg nivalenol kg bw twice a day a microbiological adaptation was seen as nivalenol metabolites (de-epoxidated nivalenol) could be found in feces and urine.

In rats and mice nivalenol showed to be toxic with adverse effects of growth retardation and leukopenia already noticed at lowest doses of 0.7 mg/kg bw per day. Lethal doses were dependent on the route of administration/intake of nivalenol. As nivalenol is normally taken up with feed the LD50 of oral administration which is 38.9 mg/kg bw per day in mice and 19.5 mg/kg bw per day in rats can be used as standard. The LD50 of intravenous, intraperitoneal and subcutaneous (SC) is between 7 and 7.5 mg/kg bw per day.

毒性の詳細 
The toxicity of nivalenol in humans is for the most parts unknown yet, but it was investigated in mice, rats and hamster cells. Thereby the toxicity was divided in the following topics: acute/subacute, subchronic, chronic and carcinogenicity, genotoxicity, developmental toxicity studies and studies on reproduction, immunotoxicity/hematotoxycity and effects on nervous system.

Acute/subacute toxicity 
The oral LD50 of nivalenol was found to be 38.9 mg/kg bw in mice whereas the intraperitonal, subcutaneous and intravenous routes of exposure gave LD50 values of 5–10 mg/kg bw. In mice already within 3 days the most deaths occurred after oral exposure through marked congestion and haemorrhage in intestine, in acute toxicity also lymphoid organs are included. Nivalenol given over time periods of 24 days in lower doses (ca. 3,5 mg/kg bw) showed significant erythropenia and slight leukopenia.

Subchronic toxicity 
The subchronic toxicity was tested by feeding mice with a daily dose of 0 to 3.5 mg nivalenol/ kg bw for 4 or 12 weeks. The observations after 4 weeks were reduced body weight and food consumption. The reduction in body weight can be explained by statistical decrease in organ weight in thymus, spleen and kidneys. Whereas the consumption time was less for female mice in comparison to male mice. After 12 weeks the toxin consumption resulted in reduction of relative organ weight in both males and females. Hereby only the liver was affected and no histopathological changes were observed.

Chronic toxicity and carcinogenicity 
Female mice were fed with different doses of nivalenol (0, 0.7, 1.4 or 3.5 mg nivalenol /kg bw) for one or two years to investigate whether nivalenol is chronic toxic and/or carcinogenic. Also during this study a decrease in body weight and feed consumption was observed. The absolute weight of both liver and kidney was decreased through the two highest doses. The mice fed for one year with nivalenol (also with the lower doses) were affected with severe leukopenia whereas the mice fed for two years had no differences in count of white blood cells. Also "no histopathological changes including tumours were found in liver, thymus, spleen, kidneys, stomach, adrenal glands, pituitary glands, ovaries, bone marrow, lymph node, brain and small intestines with or without Peyer's patch". The lowest doses (0.7 mg nivalenol /kg bw) inhibited the growth and caused leukopenia. "A no observable adverse effect level (NOAEL) could not be derived from these studies. IARC (1993) concluded that there is inadequate evidence of carcinogenicity of nivalenol in experimental animals. No human data were available. The overall conclusion was that the carcinogenicity was not classifiable (group 3)".

Genotoxicity 
It was found that nivalenol effects the genes of Chinese hamster V79 (CHO) cells by slightly increased frequencies of chromosomal aberrations and sister chromatid exchange. The DNA was damaged in CHO cells as well as in mice. In mice (given 20 mg nivalenol /kg bw orally or 3.7 mg /kg bw ip) the DNA of kidney, bone marrow, stomach, jejunum and colon was damaged. The DNA of the thymus and liver was not effected. In organs with DNA damage no necrotic changes were found upon histopathological examination. It can be concluded that an adequate evaluation of the genotoxicity is not allowed based on the available data.

Developmental toxicity and studies on reproduction 
For developmental and reproduction studies pregnant mice were injected with different amounts of purified nivalenol on days 7–15 of gestation and for one additional study with mouldy rice containing nivalenol. The studies showed that the toxin is embryotoxic in mice. No evidence of teratogenicity was given. "The LOAEL in reproduction studies with nivalenol given by oral exposure was stated to be 1.4 mg/kg bw given in the feed throughout gestation and 5 mg/kg bw when given by gavage on days 7–15". Data from other species and on reproductive effects in adult males and females are not provided yet.

Immunotoxicity/haematotoxicity 
Acute toxicity of nivalenol induces bone marrow toxicity and toxicity of lymphoid organs. Long-term exposure may result in erythropenia and/or leukopenia. In mice it was also observed that nivalenol increased the presence of serum IgA, "accompanied by immunopathological changes in kidneys analogous to human IgA-nephropathy". The blastogenesis in cultured human lymphocytes, proliferation of human male and female lymphocytes stimulated with phytoheamagglutin and pokeweed and immunoglobulin production induced by pokeweed, are inhibited by nivalenol. The effects of nivalenol are in the same range as same doses of deoxynivalenol, whereas the T-2 toxin are 100 fold more toxic. An additive effect is gained by combination of nivalenol with T-2 toxin, 4,15-diacetoxyscirpenol or deoxynivalenol.

Effects on nervous system 
About the nervous system no data has been provided yet.

関連項目 
ニバレノール、デオキシニバレノール、T2 トキシンは、いずれも真菌(Fusarium など)に天然に存在する類縁化合物である。