T 2 Toxin

466.52

466.52

244-297-7

I3FL5NM3MO

DTXSID6021298

White needles from benzene & Skellysolve B; acetate deriv: amorphous solid from ether & pentane|Crystals|White needles

29329990

121

2.27 (est)

white powder

1.3±0.1 g/cm3

151-152 °C

544.9±50.0 °C at 760 mmHg

2 °C

1.547

Freely soluble in ethyl alcohol, ethyl acetate, chloroform, DMSO, and other organic solvents; slightly sol in petroleum ether; very slightly soluble in water.

−20°C

3.06X10-11 mm Hg at 25 deg C (est)

LD50 orally in female rats: 4.0 mg/kg (Marasas); LD50 (mg/kg) in mice: 5.2 i.p., 4.2 i.v.; in rats: 7.0 intragastric, 0.9-1.3 i.p., 0.9 i.v., 2.0 s.c.; in guinea pigs: 3.0-4.0 orally, 5.3 intragastric, 1.0 i.m., 1.0-2.0 i.v., 1.0-2.0 s.c.; in pigs: 5.0 orally, 3.0 i.v. (Yagen, Bailer)

D26 +15° (c = 2.58 in ethanol)

Henry's Law constant = 5.45X10-19 atm-cu m/mole at 25 °C (est)

214 Ų [M+NH4]+ [CCS Type: TW, Method: calibrated with polyalanine]|212.51 Ų [M+Na]+

Ester groups are saponified by alkalis, and the epoxide is opened by strong mineral acids|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 3462 6.1/PG 1

3

26/27/28-38-36-20/21/22-11

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

YD0100000

T+,T,Xn,F

Stable in the solid form

P260, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P302+P352, P304+P340, P310, P320, P321, P322, P330, P332+P313, P361, P362, P363, P403+P233, P405, P501

H300

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.

Strong oxidizing agents.|Reactivity: Varies depending on the specific Toxin but generally toxins selected for warfare purposes are not exceptionally reactive to common materials. /Toxins - Dermally Hazardous/

Toxicology Review- Nutrition Reviews 31 (6): 169 (1973).|WHO; Environmental Health Criteria 105: Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot (1990)|Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)

|Danger|H300 (97.56%): Fatal if swallowed [Danger Acute toxicity, oral]|P260, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P302+P352, P304+P340, P310, P320, P321, P322, P330, P332+P313, P361, P362, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 41 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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/

Not flammable or combustible.|Fire: Toxins are not volatile but may be spread by efforts to extinguish the fire. Toxins may be decomposed by heat to produce other toxic gases. /Toxins - Dermally Hazardous/

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/

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/

T-2 toxin produces edema, intradermal hemorrhage and necrosis of the skin.

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.

LC50 Pig inhalation 1.5-3.0 mg/kg (18 hr)|LD50 Pig i.v. 1.21 mg/kg|LD50 Mice inhalation 0.16 mg/kg (24 hr)|LD50 Mice i.v. or i.p. 3.0-5.3 mg/kg|For more Non-Human Toxicity Values (Complete) data for T-2 TOXIN (11 total), please visit the HSDB record page.

/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.|/PLANTS/ ... T-2 toxin-treated seedlings exhibited dwarfism with aberrant morphological changes (e.g. petiole shortening, curled dark-green leaves, and reduced cell size). These results imply that the phytotoxic action of trichothecenes differed among their molecular species. Cycloheximide (CHX)-treated seedlings displayed neither feature, although it is known that trichothecenes inhibit translation in eukaryotic ribosomes. Microarray analyses suggested that T-2 toxin caused a defence response, the inactivation of brassinosteroid (BR), and the generation of reactive oxygen species in Arabidopsis. This observation is in agreement with our previous reports in which trichothecenes such as T-2 toxin have an elicitor-like activity when infiltrated into the leaves of Arabidopsis.

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/|Fungal source: Fusarium tricinctum; Fusarium culmorum (F roseum); Fusarium solani; Fusarium poae; Fusarium sporotrichioides; Trichoderma lignorum|A strain of Fusarium tricinctum isolated from infected corn|T-2 Toxin is a potent mycotoxin produced in feedstuffs by several species of the genus Fusarium(1,2) and Trichoderma lignorum(1).|.../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#4634]

T-2 Toxin'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 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).

A base-catalyzed second-order hydrolysis rate constant of 1.4X10-1 L/mole-sec(SRC) was estimated for T-2 Toxin using a structure estimation method(1); this corresponds to half-lives of 1.6 years and 59 days at pH values of 7 and 8, respectively(1). An estimated acid-catalyzed hydrolysis half-life for the epoxide moiety of 121 years at pH 7 was calculated(1). Trichothecenes, such as T-2 Toxin, are stable to UV light(2) and, therefore, may not be susceptible to direct photolysis by sunlight(SRC).|Stable in the solid state; ester groups are saponified by alkalis, and the epoxide is opened by strong mineral acids.

An estimated BCF of 14 was calculated in fish for T-2 Toxin(SRC), using an estimated log Kow of WWW(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 T-2 Toxin can be estimated to be 910(SRC). According to a classification scheme(2), this estimated Koc value suggests that T-2 Toxin is expected to have low mobility in soil.

The Henry's Law constant for T-2 Toxin is estimated as 5.5X10-18 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that T-2 Toxin is expected to be essentially nonvolatile from water and moist soil surfaces(2). 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(SRC), determined from a fragment constant method(3).

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).

T-2 toxin is transmitted in the milk in lactating cattle & pigs.

Occupational exposure to T-2 Toxin 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 T-2 Toxin via ingestion of contaminated food and dermal contact with consumer products containing T2-toxin. (SRC)|Trichothecenes are useful as a warfare agent because they can enter the body through the skin, by inhalation and ingestion(1). /Trichothecenes/|There is exposure to this toxin from the consumption of cereals contaminated with T2-trichothecene.

T2-Trichothecene is readily absorbed through skin & the gut in pigs & rats.|T-2 toxin is transmitted in the milk in lactating cattle & pigs.|Estimated that the eggs from chickens treated orally with 1 mg T-2 toxin/kg body weight daily for 8 consecutive days, which is equivalent to 1.6 mg/kg dietary T-2, contain 0.9 ug of this material.|The radioactivity of orally admin (3)H-T2-trichothecene (1 mg/kg body wt) to mice & rats was recovered in feces (55%) & urine (15%) within 72 hr. It was distributed in the liver, kidneys & other organs, without specific accumulation.|(3)H-T-2 Toxin given orally to mice and rats was distributed rapidly to tissues and eliminated in feces and urine. Maximal levels of radiolabel were found after 30 min in plasma of mice after oral administration ... and of guinea pigs after intramuscular injection ... . In chicks administered (3)H-T-2 toxin in the diet, maximal levels were reached by 4 hr in blood, plasma, abdominal fat, heart, kidneys, gizzard, liver and the remainder of the carcass and by 12 hr in muscle, skin, bile and gall bladder ... . The distribution of T-2 toxin in tissues of swine was similar to that in chickens ... .

Two major metabolites were obtained from the urine of a lactating cow given 180 mg of T-2 toxin orally. They were 3'-hydroxy-HT 2 toxin & 3'-hydroxy T 2 toxin.|Human liver enzymes deacetylate T2-trichothecene to HT2-trichothecene in vitro.|The radioactivity of orally admin (3)H-T2-trichothecene (1 mg/kg body wt) to mice & rats was recovered in feces (55%) & urine (15%) within 72 hr. ... Analysis of the radioactivity recovered in feces of rats revealed that 2.7% of the dose was excreted as unchanged T2-trichothecene & 7.5% as 4-O-deacetylated T2-trichothecene (HT2-trichothecene)...the remaining fecal excretion products were not identified. In urine, HT2-trichothecene, representing 1.4% of the total dose & 8-hydroxydiacetoxyscirpenol (1.8%) were identified; 3 unidentified metabolites...were also isolated. The epoxide moeity...seems to be essential for its toxicological activity; the liver detoxifies T2-trichothecene, probably through epoxide hydrolase. In vitro, rat liver homogenate metabolizes T2-trichothecene to HT2-trichothecene, T2-trichothecene tetraol, 4-deacetylneosolaniol...& neosolaniol... The same metabolites were obtained from HT2-trichothecene, indicating that T2-trichothecene was preferentially hydrolyzed at the C-4 position to give NT2-trichothecene.|Trichothecenes are sesquiterpenoid toxins produced by Fusarium species. Since these mycotoxins are very stable, there is interest in microbial transformations that can remove toxins from contaminated grain or cereal products. Twenty-three yeast species assigned to the Trichomonascus clade (Saccharomycotina, Ascomycota), including four Trichomonascus species and 19 anamorphic species presently classified in Blastobotrys, were tested for their ability to convert the trichothecene T-2 toxin to less-toxic products. These species gave three types of biotransformations: acetylation to 3-acetyl T-2 toxin, glycosylation to T-2 toxin 3-glucoside, and removal of the isovaleryl group to form neosolaniol. Some species gave more than one type of biotransformation. Three Blastobotrys species converted T-2 toxin into T-2 toxin 3-glucoside, a compound that has been identified as a masked mycotoxin in Fusarium-infected grain. This is the first report of a microbial whole-cell method for producing trichothecene glycosides, and the potential large-scale availability of T-2 toxin 3-glucoside will facilitate toxicity testing and development of methods for detection of this compound in agricultural and other products.|For more Metabolism/Metabolites (Complete) data for T-2 TOXIN (6 total), please visit the HSDB record page.

The plasma half-life for T-2 toxin is less than 20 minutes.|T-2 toxin was converted to 3'-hydroxy-HT 2 when incubated with 9000 g supernatants of human or bovine liver homogenates for 75 min at 37 °C. The metabolism of T-2 toxin was more rapid in human (20 min half-life) than in bovine (40 min half-life). The metabolite was as toxic & produced emesis almost as rapidly as T-2 toxin.

Studies with whole cells, cell-free protein synthetic system, & acid-insol cell fractions of Tetrahymena pyriformis indicated that T-2 toxin inhibited protein synthesis by impairing the 60 S ribosome subunit & inhibited RNA & dna synthesis by disturbing the cell membrane function.|T2-trichothecene binds in vitro to active SH groups of creatine phosphokinase, lactate dehydrogenase & alcohol dehydrogenase, inhibiting their catalytic activity.|The high affinity of T2-trichothecene & higher trichothecenes to SH compounds provides a molecular basis for an interaction with the spindle fiber mechanism. ...|T-2 toxin could inhibit synthesis of DNA and RNA both in vivo (0.75 mg/kg bw single or multiple doses) and in vitro (> 0.1-1 ng/mL).|For more Mechanism of Action (Complete) data for T-2 TOXIN (14 total), please visit the HSDB record page.

/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/

/SIGNS AND SYMPTOMS/ The general toxicity, hematotoxicity and immunotoxicity of T-2 toxin are considered to be the critical effects.|/CASE REPORTS/ Accidental contact of laboratory workers with crude extracts containing T2-trichothecene (approx 100 mg/L) caused severe irritation, loss of sensitivity & desquamation of skin of the hands. A soln of crude toxin caused dermatitis of the hands & face of laboratory workers.|/CASE REPORTS/ Alimentary toxic aleukia (ATA) that occurred in the USSR in the period 1941-47 was suggested to be related to the presence of Fusarium species in moldy over-wintered grain. An association to F. poae and F. sporotrichioides, which in later fungal cultures have been found to produce several trichothecenes including T-2 - and HT-2 toxin, was established. Extractions of the suspected wheat were also tested on the skin of animals, and showed toxic dermal effects. The most severe outbreak of the disease was in 1944, but outbreaks have also been reported in 1952, 1953, and 1955 particularly in people consuming over-wintered wheat. Clinical symptoms include vomiting, abdominal pain and diarrhea followed by leukopenia, bleeding from the nose and throat, depletion of the bone marrow and fever. Depending on severity necrotic lesions in the oral cavity, esophagus and stomach may occur and the lethality may be high. ATA in the second stage is characterized by leukopenia, hemorrhagic diathesis, granulopenia, bone marrow aplasia and sepsis. Although the symptoms characterizing ATA resemble symptoms seen in cats and rodents exposed to crude extracts of infected wheat or T-2 toxin, no epidemiological studies have been reported to link trichothecenes to ATA.|/CASE REPORTS/ In an outbreak of toxicosis in a Chinese county 165 subjects consumed rice infected with F. heterosporum and F. Graminearum. About 50% of the persons consuming the rice fell ill with symptoms consisting of nausea, dizziness, vomiting, abdominal distension and pain, chills and diarrhea. Samples of the suspected rice were analyzed for T-2 toxin using an ELISA assay and a level of 180-420 mg/kg was found. Analysis for other toxins was not reported. It has to be noted that these Fusarium species are not known to produce T-2 toxin, but are known to produce several other trichothecenes such as /Deoxynivalenol/ DON, nivalenol and acetyl-DON.|For more Human Toxicity Excerpts (Complete) data for T-2 TOXIN (31 total), please visit the HSDB record page.

Fusariotoxin

Type A Trichothecene

Method: EPA-OW T2 Myco; Procedure: liquid chromatography/atmospheric-pressure chemical ionization - mass spectrometry; Analyte: T-2 mycotoxins; Matrix: foodstuffs; Detection Limit: 0.1 ng/g.|The best technique to date for quantitating trichothecenes is gas liquid chromatography with electron capture or mass spectrometric detection.|A microtest plate enzyme immunoassay was developed for detection of T-2 toxin in food. The lower detection limit was 2 pg/assay.|T-2 toxin is eluted with methanol & methylene chloride from a treated ground sample, solvents removed, & residue silylated. O-trimethylsilyl deriv of T-2 toxin is detected by gas chromatography-mass spectrometry.|For more Analytic Laboratory Methods (Complete) data for T-2 TOXIN (8 total), please visit the HSDB record page.

T-2 toxin in serum, urine, & saline was determined by a modified radioimmunoassay in which the specimens were added directly to the assay tubes without extraction. Reaction between antibody & ligands was optimal at 1 hr.|Methods for the analysis of T2-trichothecene[Table#4632]