12,13-エポキシトリコテカ-9-エン-3α,4β,8α,15-テトラオール4,15-ジアセタート8-(3-メチルブタノアート)

Wear self contained breathing apparatus for fire fighting if necessary.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Protection: Evacuation: Immediately isolate an area around any liquid or solid contamination for at least 200 feet in all directions. If possible, identify the agent and develop a downwind hazard diagram ... Adjust the initial isolation distance as appropriate. Based on the type of release, amount of material aerosolized, persistence of the agent and local conditions (e.g., weather, population density, time of day), shelter-in-place until the initial cloud passes may be the most appropriate course of action since timely evacuation of the threatened downwind population may not be possible. Depending on the persistence of the agent and the potential for condensation of agent from the cloud, evacuation of the threatened population after passage of the initial cloud may be appropriate. /Toxins - Dermally Hazardous/

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.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Decontamination: Casualties/personnel: Remove potentially contaminated clothing. Wash skin with soap and water. Small Areas: Wash all surfaces with undiluted household bleach insuring a minimum contact time of 10 minutes. Wash the area with soap and water followed by rinsing with copious amounts of water. Extreme care must be exercised when dealing with dry or powdered agents as Toxins may adhere to the skin or clothing and present an inhalation hazard later. /Toxins -Dermally Hazardous/

0.0014 [mg/m3]

0.015 [mg/m3]

0.093 [mg/m3]

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Personal Protective Requirements: These Toxins pose both a severe respiratory and severe contact hazard. Toxins are generally dispersed as aerosols. Although Toxins are nonvolatile and do not pose an inhalation hazard once the aerosol has settled, residue from aerosols of Dermally Hazardous Toxins can still pose a contact threat. Wear appropriate fully encapsulating protective gear with positive pressure self-contained breathing apparatus (SCUBA). There is a significant hazard posed by contact of contaminated material with abraded skin or injection of toxins through contact with debris. Appropriate protection to avoid any potential abrasion, laceration or puncture of the skin is essential. /Toxins - Dermally Hazardous/

There are no known antidotes to trichothecene mycotoxins. Treatments are directed at supporting hemopoietic abnormalities, gastrointestinal damage, and skin damage. Administer charcoal as a slurry in case of acute oral exposure. In case of inhalation: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, Remove contaminated clothing and wash exposed area thoroughly with soap and water. (A704)

Experiments were conducted to determine the effect of dietary fibers on T-2 toxicosis in rats. Weanling rats were fed varying levels of cellulose, hemicellulose, lignin and pectin with and without T-2 toxin (3 ug/g feed) for 2 weeks. Only lignin showed promise of overcoming feed refusal and growth depression in animals fed T-2 toxin. Further experiments feeding alfalfa meal (0, 5, 10, 15, 20 or 25%) with and without T-2 toxin indicated that this lignin-rich feedstuff could largely overcome feed refusal and growth depression caused by the toxin. There was no effect of diet, however, on the activity of hepatic esterase, the enzyme believed to catabolize T-2 toxin. Rats were fed diets containing 0, 5, 12.5 or 20% alfalfa for 2 weeks and then dosed orally with [(3)H]T-2 toxin. Dietary alfalfa increased fecal excretion of 3H, whereas urinary excretion was unaffected. Residual (3)H in kidney and muscle was reduced with alfalfa feeding when [(3)H]T-2 toxin was administered orally. Residual (3)H in the digesta in the intestinal lumen increased. Alfalfa feeding was found to reduce intestinal transit time. It was concluded that the feeding of alfalfa reduced T-2 toxicosis in rats by binding the toxin in the intestinal lumen thereby promoting fecal excretion.

Active oxygen species are reported to cause organ damage. This study was therefore designed to determine whether oxidative stress contributed to the initiation or progression of hepatic DNA damage produced by T-2 toxin. The aim of the study was also to investigate the behavior of the antioxidants coenzyme Q10 (CoQ10), and alpha-tocopherol (vitamin E) against DNA damage in the livers of mice fed T-2 toxin. Treatment of fasted mice with a single dose of T-2 toxin (1.8 or 2.8 mg/kg body weight) by oral gavage led to 76% hepatic DNA fragmentation. T-2 toxin also decreased hepatic glutathione (GSH) levels markedly. Pretreatment with CoQ10 (6 mg/kg) together with alpha tocopherol (6 mg/kg) decreased DNA damage. The CoQ10 and vitamin E showed some protection against toxic cell death and glutathione depletion caused by T-2 toxin. Oxidative damage caused by T-2 toxin may be one of the underlying mechanisms for T-2 toxin-induced cell injury and DNA damage, which eventually lead to tumourigenesis.

The objective of this study was to determine whether two antioxidant vitamins, vitamins E and C, were able to counteract the production of lipid peroxides and the corresponding toxic signs of two important but diverse mycotoxins, T-2 toxin and ochratoxin A (OA). Experiment 1 was designed in a 3 x 3 factorial arrangement using three doses of vitamin E (dl-alpha-tocopheryl acetate) in the diet of Leghorn cockerels (required level according to NRC, 10x, and 100x requirements) and three toxin treatment [no toxin (Diets 1, 2, and 3), 4 mg T-2/kg of diet (Diets 4, 5, and 6), and 2.5 mg OA/kg of diet (Diets 7, 8, and 9)]. The experimental design for Experiment 2 was the same as for Experiment 1 except that Vitamin C (0, 200, and 1,000 mg/kg of diet) was used in place of vitamin E and the concentration of T-2 in Diets 4, 5, and 6 was increased to 5 mg/kg of diet. Six replicates were used per treatment with four birds per replicate. In both experiments, OA and T-2 decreased the performance of the chicks significantly. The concentration of uric acid in the plasma increased (P < 0.001) when OA was added to the diet, whereas the supplementation of the diet with vitamin E (100x the requirement) partially counteracted this effect (P = 0.07). The presence of T-2, and especially OA, in the diet decreased the concentration of alpha-tocopherol in the liver (P < 0.001). Consistent with these findings were increased values of malondialdehyde (MDA) in the liver due to OA. In Experiment 1, vitamin E supplementation partially ameliorated the prooxidative effects of OA by decreasing the concentrations of MDA (P < 0.05). These data suggest that lipid peroxides are formed in vivo by T-2 and especially by OA and that these effects can be partially counteracted by an antioxidant such as vitamin E but not by vitamin C.

The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. /These/ results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.

For more Interactions (Complete) data for T-2 TOXIN (22 total), please visit the HSDB record page.

Trichothecenes have multiorgan effects including anoerxia and weight loss, growth retardation, nervous disorders, cardiovascular alterations, immunodepression, hemostatic derangements, skin toxicity, decreased reproductive capacity, bone marrow damage, and alimentary toxic aleukia. (L1948, L1949, A2964)

LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 35 °C; Concentration: 160 ug/L for 16 hr /formulated product/

LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 30 °C; Concentration: 180 ug/L for 16 hr /formulated product/

LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 35 °C; Concentration: 160 ug/L for 24 hr /formulated product/

LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 30 °C; Concentration: 60 ug/L for 24 hr /formulated product/

For more Ecotoxicity Values (Complete) data for T-2 TOXIN (8 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 910(SRC), determined from a structure estimation method(2), indicates that T-2 Toxin is expected to have low mobility in soil(SRC). Volatilization of T-2 Toxin from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.4X10-19 atm-cu m/mole(SRC), using a fragment constant estimation method(3). T-2 Toxin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.1X10-11 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 910(SRC), determined from a structure estimation method(2), indicates that T-2 Toxin is 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 5.6X10-19 atm-cu m/mole(SRC), developed using a fragment constant estimation method(3). According to a classification scheme(4), an estimated BCF of 14(SRC), from an estimated log Kow of 2.27(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), T-2 Toxin, which has an estimated vapor pressure of 3.1X10-11 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 T-2 Toxin may be removed from the air by wet and dry deposition(SRC). Trichothecenes, such as T-2 Toxin, are stable to UV light(3) and, therefore, may not be susceptible to direct photolysis by sunlight(SRC).

T-Toxin levels were measured in 189 naturally contaminated cereal crop samples from Aba area in Sichuan Province of China. Sampling was conducted in September, 2010. The incidence of T-toxin in was 11.64% and the average level was 0.565 ug/kg; a maximum of 3.332 ug/kg was detected. The limit of detection was 0.20 ug/kg(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.

One of the first trichothecenes to be implicated in an episode of moldy corn toxicosis was T-2 Toxin; in 1972, it was reported that T-2 Toxin at the level of 2 mg/kg was present in moldy corn involved in lethal toxicosis in dairy cattle .... This event, along with increasing information regarding the acute toxicity of T-2 Toxin, prompted considerable efforts to develop methods of analysis for T-2 Toxin and the analysis of a wide range of agricultural commodities .... Only occasional samples were found to contain T-2 Toxin (incidence well below 10% in most cases), most frequently at levels <0.1 mg/kg. Usually, other trichothecenes were also found .... On the other hand, there have been isolated reports of the finding of rather high levels of T-2 Toxin, e.g., the finding of 25 mg T-2 Toxin/kg in barley ..., and 38.9 mg T-2 Toxin/kg in peanuts .... These findings, as well as reports from India of the presence of T-2 Toxin in safflower seed and sweet corn ..., and sorghum ..., and from Italy of its presence in barley, corn feed, oats, rice, and wheat ... need to be further investigated(1).

Unlike many other mycotoxins, trichothecenes do not require metabolic activation to exert their biological activity, instead directly reacting with cellular components. Trichothecenes are cytotoxic to most eukaryotic cells due to their powerful ability to inhibit protein synthesis. They do this by freely moving across the plasma membrane and binding specifically to ribosomes with high-affinity. Specifically, they interfere with the active site of peptidyl transferase at the 3'-end of large 28S ribosomal RNA and inhibit the initiation, elongation or termination step of protein synthesis, as well as cause polyribosomal disaggregation. Protein synthesis is an essential function in all tissues, but tissues where cells are actively and rapidly growing and dividing are very susceptible to the toxins. Additionally, binding to ribosomes is thought to activate proteins in downstream signalling events related to immune response and apoptosis, such as mitogen-activated protein kinases. This is known as ribotoxic stress response. Trichothecenes may also induce some alterations in membrane structure, leading to increased lipid peroxidation and inhibition of electron transport activity in the mitochondria. They can further induce apoptosis through generation of reactive oxygen species. Further secondary effects of trichothecenes include inhibition of RNA and DNA synthesis, and also inhibition of mitosis. (L1948, L1949, A2962, A2963, A2964, A2980)

Mycotoxins are harmful substances produced by fungi in several commodities with a widespread presence in foodstuffs. Human exposure to mycotoxins occurs mainly by contaminated food. The quantitation of mycotoxins in cereal-based food, highly consumed by different age population, is of concern. In this survey, 159 cereal-based samples classified as wheat, maize and rice-based, have been evaluated for the occurrence of patulin, deoxynivalenol, 3-acetyl-deoxynivalenol, fusarenon-X, diacetoxyscirpenol, nivalenol, neosolaniol, HT-2, T-2 and zearalenone by gas chromatography-tandem mass spectrometry. Intakes were calculated for average consumers among adults, children and infants and compared with the tolerable daily intakes (TDI). Data obtained were used to estimate the potential exposure levels. 65.4% of the samples were contaminated with at least one mycotoxin and 15.7% of the analyzed samples showed co-occurrence of mycotoxin. The dietary exposure to HT-2 and T-2 toxins was estimated as 0.010 and 0.086 ugkg-1bwd-1, amounting to 10% and 86% of the TDI, for adults and infants respectively. These results back up the necessity to take a vigilant attitude in order to minimize human intake of mycotoxins.

/BIRDS and MAMMALS/ Three experiments were conducted to assess mortality rate, blood chemistry, and histologic changes associated with acute exposure to T-2 mycotoxin in adult bobwhite quail. In Experiment 1, adult quail were orally dosed with T-2 toxin to determine the lethal dose that resulted in 50% mortality of the affected population (LD50), and that dose was determined to be 14.7 mg of T-2 toxin per kilogram of body weight (BW). A second experiment was performed to study the effects of 12-18 mg/kg BW T-2 toxin on blood chemistry and liver enzyme profiles. Posttreatment uric acid, aspartate aminotransferase, lactic dehydrogenase, and gamma glutamyltransferase increased as compared with pretreatment values. In contrast, posttreatment plasma total protein, cholesterol, and triglyceride levels numerically decreased as compared with pretreatment values. Changes in blood chemistry values were consistent with liver and kidney damage after T-2 toxin exposure. In Experiment 3, histologic analyses of bone marrow, spleen, liver, small intestine, kidney, and heart were conducted on birds dosed in Experiment 2. Marked lymphocyte necrosis and depletion throughout the spleen, thymus, bursa, and gut-associated lymphoid tissue in the small intestine were observed in birds dosed with 15 and 18 mg/kg BW T-2 toxin. Necrosis of liver and lipid accumulation as a result of malfunctioning hepatocytes were also observed. Little or no morphologic change was observed in bone marrow and heart tissue. The LD50 for adult bobwhite quail as found in this study is two to three times higher than that reported for other species of commercial poultry. Results from these data confirm previous reports of immunosuppressive and/or cytotoxic effects of T-2 toxin in other mammalian and avian species. T-2 toxin may have a negative impact on the viability of wild quail populations.

/AQUATIC SPECIES/ Chemical induction of apoptosis in cells is believed to contribute to toxicity. Techniques for measuring apoptosis have increased in both sensitivity and number and in many cases can be readily extended to nontraditional research species. A comparison of established assays for measuring apoptosis of lymphoid cells has thus far not been performed in the fish and thus would be efficacious in assessing immunotoxicity. The present study evaluated chemical-induced immune cell apoptosis in fish (tilapia, Oreochromis niloticus) exposed to two known immunotoxic chemicals, azathioprine and T-2 toxin. Cytocentrifugation and light microscopy of leukocyte-enriched cell samples from the pronephros (i.e., the fish primary hematopoietic compartment) demonstrated chemical-related increases in apoptotic bodies. This observation was examined further with the ApoAlert Annexin V Apoptosis kit and two DNA-binding dyes employed for detecting apoptosis, 7-aminoactinomycin D (7-AAD) and propidium iodide (PI). The apoptotic probes confirmed the microscopic observations of increased apoptosis in the chemical-exposed fish. The ApoAlerttrade mark annexin V and 7-AAD assays, which discriminate early and late apoptosis/necrosis, compared well in identifying apoptotic populations. PI staining in Vindelov's solution was unable to detect early apoptosis. The present data suggest that apoptotic immune cells may be a useful marker for certain immunotoxicant exposures in fish. These findings agree with those of previous reports that fish may respond immunologically in a manner similar to mammals after immunotoxicant challenge.

Trichothecene mycotoxin found in Fusarium tricinctum; Thought to be used in the past as a chemical warfare agent in Southeast Asia; [Merck Index] Produced by various Fusarium fungi; Human exposure has occurred from consumption of contaminated cereals; [HSDB] Produced mainly by Fusarium sporotrichioides; Occasionally found on cereals like wheat and maize; Caused mass human poisonings in Siberia in the last century; [IARC]

Implicated as a chemical warfare agent in Southeast Asia with Nivalenol.

Trichothecenes are a very large family of chemically related mycotoxins produced by various species of Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys. They are produced on many different grains like wheat, oats or maize by various Fusarium species such as F. graminearum, F. sporotrichioides, F. poae and F. equiseti. Some molds that produce trichothecene mycotoxins, such as Stachybotrys chartarum, can grow in damp indoor environments and may contribute to health problems among building occupants. T-2 Toxin is the only mycotoxin known to have been used as a biological weapon. (L1948, A735)

T2-trichothecene was first isolated ... from a culture of the fungus Fusarium tricinctum, strain T-2, by ethyl acetate extraction of the whole blended and lyophilized culture. The yield of toxin was 0.5%, based on dry weight of the lyophilized culture. There is no evidence that T2-trichothecene is produced commercially, but it can be readily prepared in gram quantities by culturing of Fusarium tricinctum on corn.

This toxin is readily produced in liquid fermentations at yields approaching 1 g/L. It can also be produced in large quantities in solid fermentations. ... T-2 toxin is produced by Fusarium sporotrichioides, F. poae, F. equiseti and F. acuminatum.