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Results for “T-2 Toxin”

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At least 19 recordsLinked to original sources
PubMed1984

Inhibition of bovine platelet function by T-2 toxin, HT-2 toxin, diacetoxyscirpenol and deoxynivalenol.

The aggregation of bovine platelets suspended in homologous plasma is inhibited in the presence of T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) or deoxynivalenol (DON) when either collagen or ADP is used as the stimulatory agent for aggregation. For each of the mycotoxins the degree of inhibition is dependent on the amount of trichothecene present in the platelet suspension but is not dependent on the time of exposure of the platelets to the toxin. For both ADP- and collagen-stimulated platelets, the order of potency of inhibition is T-2 toxin greater than HT-2 toxin greater than DAS greater than DON. A significant (P less than 0.01) dose-dependent decrease was also observed in the amount of the thromboxane B2 released from collagen-stimulated platelets in the presence of each of the mycotoxins.

Adenosine Diphosphate↗
PubMedDate not supplied

Capillary gas chromatographic determination of T-2 toxin, HT-2 toxin, and diacetoxyscirpenol in cereal grains.

A capillary gas chromatographic (GC) method using an electron capture detector is described for determining T-2 and HT-2 toxins and diacetoxyscirpenol (DAS) in cereal grains at levels as low as 100 ppb for T-2 and DAS and 50 ppb for HT-2. Samples are extracted with methanol-water according to the Scott method, and further purified on a silica gel cartridge and a cyano column. Heptafluorobutyrylimidazole (HFBI) is added to form the esters of the analytes. Ester(s) of T-2, HT-2 and DAS are separated on a 30 m X 0.32 mm DB-5 fused silica column and measured with a 63Ni electron capture detector. Samples were confirmed by gas chromatography/mass spectrometry using electron impact ionization and single ion monitoring at the molecular mass of 501.11 m/z for T-2, 665.08 m/z for HT-2, and 502.12 m/z for DAS at 10 000 resolving power. The method was applied to wheat, oats, and barley. Average recoveries ranged from a low of 65% for T-2 in barley to a high of 99% for DAS in oats.

Chromatography, Gas↗
PubMedDate not supplied

Simultaneous analysis of T-2 toxin and HT-2 toxin by an indirect enzyme-linked immunosorbent assay.

An indirect enzyme-linked immunosorbent assay (ELISA) for the detection of HT-2 toxin in the presence or absence of T-2 toxin is described. In the indirect ELISA, the relative cross-reactivities of antibodies against T-2 toxin (anti-T-2) with T-2 toxin and HT-2 toxin were 1 and 0.1, whereas anti-HT-2 cross-reactivities with T-2 toxin and HT-2 toxin were 0.33 and 1, respectively. Using such relationships, a formula was established that could be used to calculate the individual toxin concentration in a mixed sample after experimentally analyzing for T-2 and HT-2 toxins in the 2 indirect ELISAs. This method was tested by analyzing urine samples spiked with HT-2 toxin alone and samples spiked with both T-2 toxin and HT-2 toxin. A cleanup protocol for treatment of urine samples before ELISA was also established. The overall analytical recovery of HT-2 toxin when it was added at concentrations of 0.1-10 parts per billion (ppb) to the urine samples was ca 89%. When both T-2 and HT-2 toxins were added to the urine samples at equal concentrations of 0.5 to 5.0 ppb, their recoveries were 112 and 109%, respectively.

Antibody Specificity↗
PubMed1980

Synthesis of DNA in human fibroblasts treated with T-2 toxin and HT-2 toxin (the trichothecene metabolites of Fusarium species) and the effects of hydroxyurea.

(1) 3alpha-Hydroxy-4beta, 15-diacetoxy-8alpha-(3-methylbutyryloxy)-12,13-epoxytrichothec-9-ene (T-2 toxin) and HT-2 toxin both inhibited the incorporation of tritiated thymidine into the DNA of human fibroblasts; the inhibition was dose-related. (2) The presence of hydroxyurea (HU) did not affect unscheduled DNA synthesis in human fibroblasts damaged by T-2 toxin (0.006 mug/ml to 20.0 mug/ml) or by HT-2 toxin (0.032 mug/ml to 100.0 mug/ml) as with cycloheximide. (3) In the presence of the rat-liver microsomal fraction, S-9 and of hydroxyurea, there was an increase in unscheduled DNA synthesis in human fibroblasts exposed to 100 mug/ml of HT-2 toxin. (4) Thus in the presence of the microsomal S-9 fraction and of hydroxyurea the effect of HT-2 toxin (at 100 mug/ml) appeared to resemble that of benzo(a)pyrene: further studies are needed to clarify the ròle of its derivatives in the mechanism of action of T-2 toxin.

DNA↗
PubMed1988

Pharmacokinetics and protein binding of trichothecene mycotoxins, T-2 toxin and HT-2 toxin, in dogs.

The pharmacokinetics of T-2 toxin, following i.m. and i.v. administration (0.4 mg/kg), were investigated in five dogs. Following i.m. administration, the mean pharmacokinetic parameters for T-2 and HT-2 toxins were, respectively: apparent half-life 21 +/- 5 and 73 +/- 7 min; peak plasma concentration 182 +/- 42 and 74 +/- 16 ng/ml; time to reach peak plasma concentration 9.4 +/- 6.4 and 49 +/- 11 min. Mean residence time calculation, using moment analysis, showed that the terminal slope of T-2 toxin plasma levels following i.m. administration corresponds to the absorption rate constant of the toxin due to the flip-flop phenomenon. T-2 toxin was completely absorbed following i.m. administration and its absolute bioavailability was 1.17 +/- 0.25. A plasma protein binding study showed that in a concentration range of 70-500 ng/ml, T-2 and HT-2 toxins have a mean free fraction of 30.6 +/- 3.1% and 32.6 +/- 3.6% with no concentration dependency. At physiological conditions (temperature and pH), both T-2 and HT-2 toxins were unstable in whole blood and their in vitro stability half-lives were 6.9 and 0.84 hr, respectively. However, under similar conditions, these toxins were stable in plasma for 7 hr. Their instability in whole blood, therefore, may be related to enzymes present in the blood cells.

Animals↗
PubMed1975

Assay and relationship of HT-2 toxin and T-2 toxin formation in liquid culture.

Both T-2 toxin and HT-2 toxin can be conveniently quantitated in crude extracts by using a combination of thin-layer chromatography and fluorodensitometry. This technique was used to follow the production of these toxins by liquid cultures of Fusarium poae (NRRL 3287). T-2 toxin was produced prior to HT-2 toxin and hexadeuterio-T-2 toxin was converted by the culture to trideuterio-HT-2 toxin.

Chemical Phenomena↗
PubMed1984

In vitro formation of 3'-hydroxy T-2 and 3'-hydroxy HT-2 toxins from T-2 toxin by liver homogenates from mice and monkeys.

In vitro metabolism of T-2 toxin was studied in homogenates of mouse and monkey livers. In addition to several hydrolyzed products, including HT-2 toxin, neosolaniol, 4-deacetylneosolaniol, 15-deacetylneosolaniol, and T-2 tetraol, two metabolic products were isolated from the incubation mixture. Their structures were confirmed as 3'-hydroxy T-2 toxin and 3'-hydroxy HT-2 toxin on the basis of mass and nuclear magnetic resonance spectroscopy. The formation of these hydroxylated metabolites was found in the microsomes in the presence of NADPH, and the hydroxylation reaction was enhanced by treating mice with phenobarbital. The results suggest that a cytochrome P-450 is catalyzing the hydroxylation at the C-3' position of T-2 and HT-2 toxins. An in vitro metabolic pathway of T-2 toxin in the hepatic homogenates containing the NADPH-generating system is proposed.

Animals↗
PubMed1987

Production and characterization of antibodies against HT-2 toxin and T-2 tetraol tetraacetate.

Three new immunogens which were prepared by conjugation of the carboxymethyl oxime (CMO) derivatives of HT-2 toxin, T-2 tetraol (T-2 4ol), and T-2 tetraol tetraacetate (T-2 4Ac) to bovine serum albumin (BSA) were tested for the production of antibodies against the major metabolites of T-2 toxin. Antibodies against HT-2 toxin and T-2 4Ac were obtained from rabbits 5 to 10 weeks after immunizing the animals with CMO-HT-2-BSA and CMO-T-2 4Ac-BSA conjugates. Immunization with CMO-T-2 4ol-BSA resulted in no antibody against T-2 4ol. The antibody produced against HT-2 toxin had great affinity for HT-2 toxin as well as good cross-reactivity with T-2 toxin. The relative cross-reactivities of anti-HT-2 toxin antibody with HT-2 toxin, T-2 toxin, iso-T-2 toxin, acetyl-T-2 toxin, 3'-OH HT-2, 3'-OH T-2, T-2 triol, and 3'-OH acetyl-T-2, were 100, 25, 10, 3.3, 0.25, 0.15, 0.12 and 0.08%, respectively. Antibody against CMO-T-2 4Ac was very specific for T-2 4Ac and had less than 0.1% cross-reactivity with T-2 toxin, HT-2 toxin, acetyl-T-2 toxin, diacetoxyscirpenol, deoxynivalenol, and deoxynivalenol triacetate as compared with T-2 4Ac. The detection limits for HT-2 toxin and T-2 4ol by radioimmunoassay were approximately 0.1 and 0.5 ng per assay, respectively.

Animals↗
PubMedDate not supplied

HPLC: a tool for the analysis of T-2 toxin and HT-2 toxin in cereals.

An analytical procedure for the determination of trichothecenes in various cereals is described. HPLC was performed with a reversed-phase (C18) column eluted with methanol:water (60:40, v/v). Compounds were detected with a refractive index detector. The elution patterns of free and contaminated samples were compared. The recovery of added T-2 toxin (2 and 5 micrograms/g) in rye and wheat was approximately 80%. The application of this method allows for combined use with other sensitive methods such as mass spectrometry and gas chromatography. The described method is operationally simple, relatively inexpensive, and requires no derivatization.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Pharmacokinetics of T-2 toxin and its metabolite HT-2 toxin, after intravenous administration in dogs.

The pharmacokinetics of T-2 toxin and HT-2 toxin were investigated comparatively in five dogs, after iv administration of the toxins (0.4 mg/kg). T-2 toxin was very rapidly and almost completely biotransformed to HT-2 toxin (fm = 83.6 +/- 3.9%). The following mean pharmacokinetic parameters were determined in this study for T-2 toxin and HT-2 toxin, respectively: half-life 5.3 +/- 2.1 and 19.6 +/- 4.7 min, clearance 0.107 +/- 0.056 and 0.167 +/- 0.074 liters/min/kg, and volume of distribution 0.86 +/- 0.63 and 4.47 +/- 1.38 liters/kg. The high clearance values suggest that the metabolism of T-2 toxin and HT-2 toxin is carried out in blood and/or through diffusion by nonspecific carboxyesterases. The results of this study suggest the possibility of a sustenance of T-2 toxin metabolism by its binding to blood cells.

Animals↗
PubMed1998

An unusual case of microangiopathic haemolytic anaemia associated with enterohaemorrhagic Escherichia coli O113:H21 infection, a verocytotoxin-2/shiga toxin-2 producing serotype.

A case of microangiopathic haemolytic anaemia and thrombocytopaenia in a 79-year-old woman is presented. The case is unusual in that diarrhoeal symptoms were brief and symptoms of anaemia caused her to re-present to hospital 6 days after the diarrhoea had ceased. Enterohaemorrhagic Escherichia coli O113:H21 producing shiga toxin-2 was isolated from a faecal specimen. This serotype has been reported only a few times to be associated with serious disease. However, it is amongst the 20 most common serotypes carried in cattle and found in beef. This case also illustrates the importance of using shiga-toxin gene detection in faecal cultures (as opposed to cultural methods for detection of the O157:H7 serotype) as the recommended investigation of human disease for accurate epidemiology and attribution of cause.

Aged↗
PubMed1990

Modulation of resistance to mastitis pathogens by pretreatment of mice with T-2 toxin.

T-2 toxin, a secondary metabolite of Fusarium species, is a mycotoxin with immunomodulatory activity. In the present investigation the effects of T-2 toxin on host resistance was studied. The virulence of Escherichia coli and Staphylococcus aureus in the mammary glands of mice treated with T-2 toxin was compared with their virulence in control mice. Virulence was estimated from the ability to induce various types of lesions and bacterial growth in the mammary gland. Pretreatment of mice with a single dose (3 mg/kg body weight) of T-2 toxin by gavage reduced the virulence of both E. coli (P less than 0.05) and S. aureus (P less than 0.01). Microscopic lesions in the infected glands varied in character, from consistently non-reactive necrosis of the entire mammary gland to limited inflammatory reactions. The former were more abundant in control mice than in mice treated with T-2 toxin. Although treatment by gavage with T-2 toxin (0.75 mg/kg body weight/day) for 14 days prior to inoculation had no significant effect on the course of the mastitis infection, virulence was slightly lower in the T-2 toxin treated mice. Both single-dose and successive treatment with T-2 toxin enhanced the respiratory burst activity of macrophages. Pre-inoculation treatment with T-2 toxin also caused a significant increase in the number of peritoneal cells, T-2 toxin did not show bacterial effects on the E. coli or S. aureus strains used for the inoculations. The data indicate that T-2 toxin has modulatory effects on the cell-mediated immune system, and that enhancement of resistance to common mastitis pathogens in mice pretreated with a single dose of T-2 toxin is associated with migration and activation of macrophages.

Animals↗
PubMed1985

Structures of deepoxytrichothecene metabolites from 3'-hydroxy HT-2 toxin and T-2 tetraol in rats.

3'-Hydroxy HT-2 toxin and T-2 tetraol, in vivo metabolites of T-2 toxin, were orally administered to Wistar rats, and four metabolites having a trichothec-9,12-diene nucleus, which were termed deepoxytrichothecenes, were newly found in the excreta. Their structures were confirmed as 3'-hydroxy-deepoxy HT-2, 3'-hydroxy-deepoxy T-2 triol, 15-acetyl-deepoxy T-2 tetraol, and deepoxy T-2 tetraol on the basis of mass and nuclear magnetic resonance spectroscopy. Resolution of T-2 metabolites and corresponding deepoxytrichothecenes by gas-liquid and thin-layer chromatography was also described.

Animals↗
PubMed1999

An IL-2-toxin, DAB389IL-2, inhibits delayed-type hypersensitivity but enhances IgE antibody production.

BACKGROUND: Expression of high-affinity IL-2 receptor (IL-2R) on T lymphocytes, key cells in chronic inflammation, is a T-cell activation marker. OBJECTIVE: We sought to evaluate the effect of the fusion protein DAB389IL-2, which kills cells bearing IL-2R, on delayed-type hypersensitivity and antibody production in Brown Norway rats sensitized with trimellitic anhydride (TMA). METHODS: DAB389IL-2 (25 micrograms/kg/day) or placebo was administered intraperitoneally for 8 days over the period of sensitization, starting 2 days before sensitization. RESULTS: The administration of DAB389IL-2 resulted in a one-third reduction in the number of IL-2R-bearing cells and significant weight loss of animals. Delayed-type hypersensitivity, evaluated at 5 weeks after sensitization, was significantly inhibited by treatment with DAB389IL-2. In contrast, production of IgE anti-TMA antibodies after sensitization was increased by treatment with DAB389IL-2. DAB389IL-2 affected neither IgG anti-TMA antibody nor total IgE levels. CONCLUSION: These data imply that systemic administration of DAB389IL-2 in Brown Norway rats influences cells that have regulatory effects on the immune system, resulting in a switch from a TH1 to a TH2 type of immune response.

Allergens↗
PubMed2000

In vitro inhibitory effects of antioxidants on cytotoxicity of T-2 toxin.

T-2 toxin is a secondary fungal metabolite produced by various species of Fusarium. It is capable of killing cells by causing extensive damage to the cellular membrane. In this study, cytotoxicity of T-2 toxin in combination with different antioxidant materials, including vitamin C (vit. C), vitamin E (vit. E) and selenium (sel) was investigated in vitro using the neutral red cytotoxicity assay. Eleven primary and transformed cell lines established from different tissues were used in pre-test experiments to identify the most sensitive and resistant lines by measuring the half lethal concentration (LC(50)) of the toxin. Three cell lines including human gingival fibroblast (HGF), the most sensitive (LC(50)=0.25 ng/ml), human colorectal adenocarcinoma (SW742), the most resistant (LC(50)=5.5 ng/ml) and human hepatoma (HepG2), with median susceptibility (LC(50)=2 ng/ml) were selected to investigate the inhibitory effects of the antioxidant agents, on cytotoxicity of T-2 toxin. Our results demonstrated that co-incubation of cell lines with different concentrations of T-2 toxin and antioxidants decreased significantly, but did not totally inhibit, the cytotoxicity of T-2 toxin (P<0.001). These findings suggest that in addition to lipid peroxidation, which is inhibited by antioxidants, other unidentified mechanism(s) seem to be involved in cytotoxicity of T-2 toxin.

Antioxidants↗