Nivalenol

312.32

312.32

200-835-2

DTXSID3021067

Crystals from methanol|Crystals

38220090

119.75000

-0.75

white crystalline powder

1.6±0.1 g/cm3

222-223 °C (decomp)

585.1±50.0 °C at 760 mmHg

2 °C

1.658

In water, 3.54X10+5 mg/L at 25 °C (est)|Soluble in polar organic solvents

2-8°C

3.98E-16mmHg at 25°C

LD50 i.p. in mice: 40 mg/10 g (Tatsuno)

24D +21.54° (c = 1.3 in ethanol)

Henry's Law constant = 7.33X10-16 atm-cu m/mole at 25 °C (est)

Colorless, mostly crystalline solids that have been well characterized by physical and spectroscopic techniques. ... require higher polarity solvents, such as aqueous methanol or aqueous acetonitrile. /Trichothecenes/|The trichothecenes are generally stable; for example, DON (deoxynivalenol) can be stored in organic solvents, such as ethyl acetate, for a long time without any significant deterioration ... They remain unaffected when refluxed with various organic solvents and also under mildly acidic conditions.

I

6.1(a)

UN 2811 6.1/PG 1

3

26/27/28-36-20/21/22-11

22-36/37/39-45-36/37-26-28-16

YD0165000

T+,Xn,F

Stable under recommended storage conditions.

P210-P305 + P351 + P338

H225-H302 + H332-H319

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

/Avoid/ Heat, flames and sparks. Extremes of temperature and direct sunlight.

Saito M, Tatsuno T; Toxins of Fusarium nivale; Microbial toxins 7: 293 (1971). A review with 75 ref. The toxic effects of nivalenol produced by F nivale and related species on livestock and humans, and the phys, chem, and carcinogenic properties of these compd are discussed.|WHO; Environmental Health Criteria 105: Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot (1990)|WHO ENVIRONMENTAL HEALTH CRITERIA 11: MYCOTOXINS WHO GENEVA SWITZERLAND ILLUS PAPER ISBN 92-4-154071-0 0(0) 127 PAGES (1979) A review on toxicity of mycotoxins to humans and animals, incl nivalenol.|Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)

|Danger|H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]|P260, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P304+P340, P310, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 39 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Vapors may form explosive mixture with air.|Flammable in the presence of a source of ignition when the temperature is above the flash point. Keep away from heat/sparks/open flame/hot surface. No smoking.

Wear self contained breathing apparatus for fire fighting if necessary.|Use water spray to cool unopened containers.|Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Contain spillage, and then collect with an electrically protected vacuum cleaner or by wet-brushing and place in container for disposal according to local regulations

Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Remove all sources of ignition. Evacuate personnel to safe areas. Beware of vapors accumulating to form explosive concentrations. Vapors can accumulate in low areas.

Trichothecenes are well known skin irritants and nivalenol has been shown in some early studies to have weak skin irritancy properties.

A feeding trial was conducted in order to determine the effects of a Fusarium poae extract on the health and performances of broiler chickens and the possible protective effect of a natural zeolite. The F. poae extract contained nivalenol, T-2 toxin and diacetoxyscirpenol and demonstrated high toxicity when administered i.p. to rats. One-day-old broiler chickens were fed ad libitum over a period of 28 days with the following diets: group I - control; group II - 0.5% zeolite; group III -F. poae extract; group IV-0.5% zeolite andF. poae extract. Broilers were sacrificed at 28 days for the measurement of relative organs weights, leukocyte counts and serum biochemical values. No mortality was recorded over the experiment. Body weight gains, feed intake, feed utilization and water consumption were depressed by the F. poae extract (p<0.05). A decrease of these parameters was also observed in group IV which received the diet with zeolite and the F. poae extract. No significant differences were seen in group II when compared to control. In groups III and IV the relative weights of liver, kidney, heart and gizzard were significantly increased (p<0.05), while in group II only the relative liver weight was increased. F. poae extract, administered singly or in combination with zeolite, significantly decreased leukocytes count, serum total protein and serum albumin. Zeolite and F. poae extract, singly or combined, increased serum creatinine and uric acid concentrations (p<0.05). These findings indicate that sublethal doses of F. poae extract can affect adversely the performances and the health in broiler chickens. By adding zeolite these impairments could not be diminished and for some parameters the zeolite additive increased the adverse effects of the F. poae extract.|Deoxynivalenol (DON) and nivalenol (NIV) are toxic Fusarium secondary trichothecene metabolites that often co-occur regularly in cereal grains. These compounds were compared for their toxicity towards C57BL/6 mice on several parameters including alteration in plasma biochemistry, immune system reactivity and hepatic drug metabolism capacity. Mice received individual or combined oral doses of each toxin: 0.071 or 0.355 mg/kg of body weight, administrated three days a week for 4 weeks. Food consumption was altered by the single administration of 0.355 mg/kg of NIV, although no noticeable change of body and organ weights or liver protein contents was detected. NIV administration did cause also significant changes in total CO2 and uric acid concentrations in plasma. Individual toxin exposures led to increases in plasma IgA without no detectable change in the ex vivo production of cytokine by splenocytes. The liver ethoxyresorufin O-deealkylase, pentoxyresorufin O-depenthylase and glutathione S-transferase activities were increased in concert with cytochrome P4501a and P4502b subfamily expression. Administration of combinations of DON and NIV resulted in responses similar to that observed using individual doses of each toxin. However, depending on the ratio of toxin doses and biochemical parameters, some responses could be also additive (plasma IgA and hepatic DCNB conjugation) or synergistic (plasma uric acid).|Deoxynivalenol (DON) is the most prevalent trichothecene mycotoxin in crops in Europe and North America. DON is often present with other type B trichothecenes such as 3-acetyldeoxynivalenol (3-ADON), 15-acetyldeoxynivalenol (15-ADON), nivalenol (NIV) and fusarenon-X (FX). Although the cytotoxicity of individual mycotoxins has been widely studied, data on the toxicity of mycotoxin mixtures are limited. The aim of this study was to assess interactions caused by co-exposure to Type B trichothecenes on intestinal epithelial cells. Proliferating Caco-2 cells were exposed to increasing doses of Type B trichothecenes, alone or in binary or ternary mixtures. The MTT test and neutral red uptake, respectively linked to mitochondrial and lysosomal functions, were used to measure intestinal epithelial cytotoxicity. The five tested mycotoxins had a dose-dependent effect on proliferating enterocytes and could be classified in increasing order of toxicity: 3-ADON<15-ADON =~ DON

LD50 Mouse oral 38.9 mg/kg|LD50 Mouse ip 7.4 mg/kg|LD50 Mouse sc 7.2 mg/kg|LD50 Mouse iv 7.3 mg/kg|For more Non-Human Toxicity Values (Complete) data for NIVALENOL (6 total), please visit the HSDB record page.

Freshly harvested wheat and barley of the 1977 crop were examined for trichothecene mycotoxin contamination and for the presence of Fusarium species. Trichothecenes, such as nivalenol, were not detected in these samples. The incidence of Fusarium contamination ranged from 0-32.7%. The most common species was F. graminearum. Among 57 isolates of F. graminearum, 43 produced nivalenol.|Fungi from the genus Fusarium, growing on barley, corn, oats, rye, or wheat, produce dozens of derivatives of tetracyclic sesquiterpenes are called trichothecenes. The best known of these mycotoxins are nivalenol, deoxynivalenol, diacetoxyscirpenol, and T-2 Toxin. /Trichothecenes/|.../Trichothecene/ compounds are produced primarily by moulds belonging to the genus Fusarium, though other genera, including Trichoderma, Trichothecium, Myrothecium, and Stachybotrys, are also known to produce metabolites now characterized as trichothecenes. Only a few of the known trichothecenes have been found to contaminate food or animal feed ... (1). /Trichothecenes/[Table#4625]

/OTHER TOXICITY INFORMATION/ Grains and grain-based foods made the largest contribution to the nivalenol exposure /in humans/. Important contributors were bread and rolls, grain milling products, pasta, fine bakery wares, and breakfast cereals. The contribution of bread and rolls is due to high consumption, while the contribution of grain milling products is likely due to several high nivalenol concentration values.|Nivalenol's use as a biological agent(1) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that nivalenol is expected to have very high mobility in soil(SRC). Volatilization of nivalenol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 7.3X10-16 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Nivalenol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.9X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2013).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that nivalenol is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 7.3X10-16 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of -2.24(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2013).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), nivalenol, which has an estimated vapor pressure of 6.9X10-13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase nivalenol may be removed from the air by wet and dry deposition(SRC). Trichothecenes, such as nivalenol, are stable to UV light(4) and, therefore, may not be susceptible to direct photolysis by sunlight(SRC).

An acid-catalyzed second-order hydrolysis rate constant of 1.2X10-3 L/mole-sec(SRC) was estimated for the epoxide moiety of nivalenol using a structure estimation method(2); this corresponds to a half-life of 185 years at pH values of 7(1). Trichothecenes, such as nivalenol, are stable to UV light(2) and, therefore, may not be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for nivalenol(SRC), using an estimated log Kow of -2.24(1) and a regression-derived equation(1)). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of nivalenol can be estimated to be 10(SRC). According to a classification scheme(2), this estimated Koc value suggests that nivalenol is expected to have very high mobility in soil.

The Henry's Law constant for nivalenol is estimated as 7.3X10-16 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that nivalenol is expected to be essentially nonvolatile from water and moist soil surfaces(2). Nivalenol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 6.9X10-13 mm Hg(SRC), determined from a fragment constant method(3).

Nivalenol was not detected in four cassava flour, fifteen peanut cake nor four maize samples from local markets in the Republic of Benin, sub-Saharan Africa. Limit of detection in maize, cassava (Manihot esculata), and peanut cake was 35, 31, and 25 ug/kg, respectively(1).|In the present study, the occurrence of eighteen mycotoxins, nine trichothecenes (deoxynivalenol, 3-acetyl-deoxynivalenol, 15-acetyl-deoxynivalenol, nivalenol, neosolaniol, diacetoxyscirpenol, fusarenon-X, T-2 toxin and HT-2 toxin), three zearalenones (zearalenone, alpha-zearalenol and beta-zearalenol), and six emergent mycotoxins, beauvericin and five enniatins (A, A1, B, B1 and B4), was monitored in different Italian organic cereals and cereal products by using a liquid chromatography coupled to triple quadrupole mass spectrometry method. A total of 93 organic cereal samples (wheat, barley, rye and oat) were collected from Italy. Limits of quantification ranged from 5 to 15 ug/kg. 80% of analyzed samples contained mycotoxins. The occurrence was 33%, 6.5%, 2%, 27%, 7%, 10% and 43% for deoxynivalenol, HT-2, T-2, nivalenol, zearalenone, beauvericin and enniatins, respectively. The major mycotoxin found was enniatin B4; it was detected in 40% of all analyzed samples and its levels ranged from 5.7 to 284.2 ug/kg. Risk assessment was evaluated by EDI calculations which were lower than TDI for all legislated Fusarium mycotoxins.|Natural occurrence of nivalenol in cereals and foods sampled worldwide from 1980-1985(1).[Table#4624]

Occupational exposure to nivalenol may occur through inhalation and dermal contact with this compound at workplaces where grain is handled or processed. Monitoring data indicate that the general population may be exposed to nivalenol via ingestion of contaminated food and dermal contact consumer containing nivalenol. (SRC)

Nivalenol is rapidly distributed to and eliminated from all examined tissues in mice with no apparent accumulation in any organ.|After long term oral administration of nivalenol to male rats, the dose was recovered as fecal nivalenol (7%), fecal de-epoxy nivalenol (80%), urinary nivalenol (1%) and urinary de-epoxy nivalenol (1%).|In order to investigate the comparative fates of nivalenol (NIV) and 4-acetyl derivative of NIV (fusarenon-X, FX) in mice, (3)H-FX or (3)H-NIV was given p.o. to mice. Radioactivity was excreted mainly via the urine in mice given (3)H-FX, but mainly via the feces in mice given (3)H-NIV. The plasma radioactivity reached a peak at 30 or 60 min after the administration of (3)H-FX or (3)H-NIV, respectively. The plasma peak level was 5 times higher, and the area under curve (AUC) was 10 times higher, in (3)H-FX-administered than (3)H-NIV-administered mice. These findings clearly demonstrate that FX is absorbed from the gastrointestinal tract more rapidly and efficiently than NIV. The HPLC profile of radioactivity of acetonitrile extracts of urine and feces indicated that FX is rapidly metabolized to NIV after being absorbed from the gastrointestinal tract. In vitro incubation of tissue homogenates with (3)H-FX demonstrated that the liver and kidney are the organs responsible for the FX-to-NIV conversion. Thus this study demonstrated that the higher oral toxicity of FX than NIV that has been observed in mice and rats is due to the efficient absorption of FX than NIV from the gastrointestinal tract, followed by its rapid conversion to NIV by the liver and kidney.

There is evidence of major species-dependent differences in the extent of de-epoxidation of nivalenol in non-ruminants, which may occur in the lower parts of the gastrointestinal tract in some species. The de-epoxy metabolite has been detected in feces of rats, pigs and laying hens, but not in mice or broiler chickens and, based on in vitro studies, it is unlikely to be formed in humans.|In ruminants, it is likely that, as for other trichothecenes, extensive de-epoxidation of nivalenol may occur in the rumen prior to absorption.|Nivalenol is metabolized to de-epoxy nivalenol.|The cytotoxicity of the de-epoxy metabolites of trichothecenes nivalenol (NIV) and deoxynivalenol (DON) was determined and compared with the cytotoxicity of the respective toxin with an intact epoxy group and their acetylated derivatives. The cytotoxic effects was determined by using the 5-bromo-2'-deoxyuridine (BrdU) incorporation assay assessing DNA-synthesis. The toxicity of NIV and DON expressed as the concentration inhibiting 50% of the DNA synthesis (IC(50)), was occurring at similar micromolar concentrations (1.19+/-0.06 and 1.50+/-0.34 uM). The toxicity of fusarenon X (4-acetyl NIV) in the assay was similar to the toxicity of NIV, and the toxicity of 15-AcDON was equal to the toxicity of DON. 3-AcDON was less toxic than DON and 15-AcDON. The IC(50) value for de-epoxy DON was 54 times higher in the assay than the IC(50) for DON, while the IC(50) of de-epoxy NIV was 55 times higher than the IC(50) for NIV. The results verify previous findings that the de-epoxidation is a detoxification reaction.

Trichothecenes, such as nivalenol, inhibit peptidyl transferase with subsequent inhibition of peptide bond formation. The target organelle of trichothecene action is the 60S subunit of eukaryotic ribosomes, the protein inhibition activity correlating well with ribosome affinity. The mechanism of protein inhibition can be of two types: one is the inhibition of the initial step of protein synthesis (I-type) and the other the inhibition of the elongation-termination step (ET-type). Nivalenol is acting on the initial step of protein synthesis with an ID50 of 2.5 mg/mL in rabbit reticulocytes . Being potent direct and indirect inhibitors of protein, deoxyribonucleic (DNA) and ribonucleic (RNA) acids synthesis, trichothecenes are especially toxic to tissues with a high cell proliferation rate.|Nivalenol rapidly inhibited protein synth both in HELA cells and in yeast spheroblasts. Nivalenol was a potent and highly selective inhibitor of polypeptide chain initiation in eukaryotes.|Deoxynivalenol (DON) and nivalenol (NIV), trichothecene mycotoxins, are secondary metabolites produced by Fusarium fungi. Trichothecene mycotoxins cause immune dysfunction, thus leading to diverse responses to infection. The present study evaluated the effect of DON and NIV on nitric oxide (NO) production by RAW264 cells stimulated with lipopolysaccharide (LPS). LPS-induced NO production was reduced in the presence of these toxins. The transcriptional activation and expression of inducible NO synthase (iNOS) by LPS were also repressed by these toxins. DON or NIV inhibited LPS-induced expression of interferon-beta (IFN-beta), which plays an indispensable role in LPS-induced iNOS expression. These results indicate that DON and NIV inhibit the LPS-induced NO and IFN-beta production, which both play an important role for host protection against invading pathogens, and suggests that the inhibition of these factors may be involved in the immunotoxic effects of these mycotoxins.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|Emergency and supportive measures. 1. Provide aggressive supportive care. Treat hypotension with IV fluids and vasopressors and respiratory failure with assisted ventilation. 2. Isolate patients with suspected plague, smallpox, or viral hemorrhagic fevers, who may be highly contagious. Patient isolation is not needed for suspected anthrax, botulism, or tularemia because person-to-person transmission is not likely. However, health care workers should always use universal precautions. /Warfare agents-biological/|Decontamination. NOTE: The clothing and skin of exposed individuals may be contaminated with spores, toxin, or bacteria. rescuers and health care providers should take precautions to avoid secondary contamination. 1. Remove all potentially contaminated clothing and wash the patient thoroughly with soap and water. 2. Dilute bleach (0.5%) and ammonia are effective for cleaning surfaces possibly contaminated with viruses and bacteria. 3. All clothing should be cleaned with hot water and bleach. /Warfare agents-biological/

/CASE REPORTS/ Human toxicosis related to ingestion of Fusarium infected grain (Scabby grain diseases) was previously reported in several countries, including Japan and Korea during the period of 1946-1963, and India ...nausea, vomiting, diarrhea and abdominal pain were common symptoms associated with the toxicosis, recovery usually occurred within a few days and no lethal cases were reported. Typically mixtures of trichothecenes were detected but no single toxin could be identified as being solely responsible for the toxicosis. In the outbreaks in Japan and Korea, F. graminearum was isolated from suspected cereals suggesting a possibility of deoxynivalenol and/or nivalenol contamination. The number of cases involved was over 100 in both the two Chinese and the two Indian outbreaks, although none was lethal. In 1987, an acute outbreak in India affecting approximately 50,000 people was due to consumption of bread made from rain-damaged wheat. The wheat contained deoxynivalenol (0.34-8.4 mg/kg in 11 of 24 samples), acetyldeoxynivalenol (0.6-2.4 mg/kg in 4 of 24 samples), nivalenol (0.03-0.1 mg/kg in 2 of 24 samples) and T-2 toxin (0.55-4.0 mg/kg in 3 of 24 samples). Cases exhibited mainly minor gastrointestinal symptoms (abdominal pain, diarrhea, bloody stool and vomiting) for approximately two days.|/BIOMONITORING/ Fusarium species are probably the most prevalent toxin-producing fungi of the northern temperate regions and are commonly found on cereals grown in the temperate regions of America, Europe and Asia. Among the toxins formed by Fusarium /the authors/ find trichothecenes of the A-type or B-type, zearalenone, fumonisins or nivalenol. The current exposure assessment consists of the qualitative and/or quantitative evaluation based on the knowledge of the mycotoxin occurrence in the food and the dietary habits of the population. This process permits quantifying the mycotoxin dietary intake through deterministic or probabilistic methods. Although these methods are suitable to assess the exposure of populations to contaminants and to identify risk groups, they are not recommended to evaluate the individual exposition, due to a low accuracy and sensitivity. On the contrary, the use of biochemical indicators has been proposed as a suitable method to assess individual exposure to contaminants. In this work, several techniques to biomonitor the exposure to fumonisins, deoxynivalenol, zearalenone or T-2 toxin have been reviewed.|/GENOTOXICITY/ This study aims to assess the genotoxic potential of nivalenol (NIV) and fusarenon X (FusX), produced by various Fusarium on cereals. Toxins were applied in time and dose-dependent experiments to the human enterocyte-like Caco-2 cell-line, both in dividing (undifferentiated) and in 10-12 days post-confluent cells (differentiated). Genotoxicity was evaluated through the alkaline Comet assay in a concentration range defined for each toxin as below the cytotoxicity threshold IC(10), determined by the MTS and the neutral red assays, to prevent false positive results because of DNA damage stemming from necrosis. Thus, genotoxicity was explored in the sub-cytotoxic 0-0.5 uM and 0-0.05 uM ranges respectively for NIV and FusX as the latter was found about 10-fold more cytotoxic than NIV. For both toxins, a 3hr exposure did not cause any DNA damage, unlike after 24 and 72 hr exposure in post confluent Caco-2 cells where DNA damage was significantly observed with a dose-dependent relationship. In dividing cells, only FusX increases DNA strand breaks in the 0.01-0.05 uM range after 72 hr. These results demonstrated the existence of a genotoxic potential for NIV and FusX at low exposure levels and could contribute to the risk assessment process of these toxins that are of growing concern.|/ALTERNATIVE and IN VITRO TESTS/ Nivalenol was toxic to HELA and L (mouse fibroblasts) cells.|For more Human Toxicity Excerpts (Complete) data for NIVALENOL (14 total), please visit the HSDB record page.

nivalenol

TLC detection: brown color with sulfuric acid spraying & heating at 110 °C for 5 min.|Detection limit was 2 ng/injection in HPLC method. The method appears to be adequate for the detection of trichothecenes in contaminated corn and rice as well as in cultures of fusarium.|The best technique to date for quantitating trichothecenes was GLC with electron-capture of mass spectrometric detection, subject to available instrumentation.|A gas-liq chromatography method for determination of trichothecenes, toxic metabolites from fusarium, was developed. Nivalenol and its related compd were completely converted by use of a mixt of n-trimethylsilylimidazole.|For more Analytic Laboratory Methods (Complete) data for NIVALENOL (9 total), please visit the HSDB record page.