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T-2 Tetraol Sale

(Synonyms: T-2 四醇) 目录号 : GC44980

A metabolite of T-2 toxin

T-2 Tetraol Chemical Structure

Cas No.:34114-99-3

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100μg
¥1,113.00
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1mg
¥6,682.00
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产品描述

T-​2 Tetraol is a metabolite of T-2 toxin, and also a trichothecene mycotoxin, with less toxicity and is unable to induce apoptosis[1][2].

References:
[1]. Engler KH, et al. A colorimetric technique for detecting trichothecenes and assessing relative potencies. Appl Environ Microbiol. 1999 May;65(5):1854-7.
[2]. Islam Z, et al. Structure-function relationship of T-2 toxin and its metabolites in inducing thymic apoptosis in vivo in mice. Biosci Biotechnol Biochem. 1998 Aug;62(8):1492-7.

Chemical Properties

Cas No. 34114-99-3 SDF
别名 T-2 四醇
Canonical SMILES CC1=C[C@]2([H])[C@]([C@]([C@H](O)[C@H]3O)(C)[C@@]4(OC4)[C@]3([H])O2)(CO)C[C@@H]1O
分子式 C15H22O6 分子量 298.3
溶解度 Dichloromethane: 10 mg/ml 储存条件 Store at -20°C
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1 mM 3.3523 mL 16.7616 mL 33.5233 mL
5 mM 0.6705 mL 3.3523 mL 6.7047 mL
10 mM 0.3352 mL 1.6762 mL 3.3523 mL
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Research Update

Stability of T-2, HT-2, and T-2 Tetraol in biological fluids

J Anal Toxicol 1988 Jan-Feb;12(1):48-50.PMID:3352243DOI:10.1093/jat/12.1.48.

The stabilities of tritium-labeled T-2, HT-2, and T-2 Tetraol were studied in blood and urine at -70 degrees, 4 degrees, and 23 degrees C for 6 months in the presence of EDTA or NaF. Samples were counted with a radiochromatographic scanner and results indicated the stability of T-2 Tetraol greater than T-2 greater than HT-2. Toxins were most stable when stored at -70 degrees C, in the presence of NaF, and in urine (pH 6). They were less stable in saline (control, pH 7) and least stable in blood (pH 8). These results suggest that urine and T-2 Tetraol are the biological fluid and metabolite of choice for diagnostic purposes.

Pharmacokinetics of T-2 Tetraol, a urinary metabolite of the trichothecene mycotoxin, T-2 toxin, in dog

Xenobiotica 1987 Aug;17(8):941-50.PMID:3673109DOI:10.3109/00498258709044192.

1. The urinary metabolites of T-2 toxin were identified and analysed quantitatively after i.v. administration to dogs. 2. A new routine assay for T-2 Tetraol was developed and a pharmacokinetic study was carried out on this final hydrolytic metabolite of T-2 toxin. T-2 Tetraol was excreted in urine for 2-3 days. Its 'sigma minus' plot demonstrated a significantly longer apparent half-life than its precursors (T-2 toxin and HT-2 toxin). This fact was explained by extraplasma binding causing prolongation of the metabolism and excretion of T-2 toxin metabolites. 3. The urinary metabolites of T-2 toxin were: HT-2 toxin, T-2 triol and T-2 Tetraol. The metabolites were excreted in free and conjugated forms. In two dogs T-2 toxin was found in the urine in an amount which accounts for 3.2 and 16% of the administered dose respectively. The cumulative amount of the identified metabolites and toxins formed in the urine ranged from 9.7 to 17.3% in four dogs and 44.7% in one dog.

T-2 Tetraol is cytotoxic to a chicken macrophage cell line

Poult Sci 1997 Feb;76(2):311-3.PMID:9057211DOI:10.1093/ps/76.2.311.

Cytotoxic effects of T-2 Tetraol, a T-2 toxin derivative, on the MQ-NCSU chicken macrophage cell line were quantified by direct in vitro exposure. Macrophage cultures were exposed to 1, 10, 20, 40, 80, 160, and 320 micrograms/mL of T-2 Tetraol for 1 h. Macrophage viability after exposure to T-2 Tetraol. Macrophage viability was reduced by increasing concentrations of T-2 Tetraol (linear effect, P < or = 0.001; quadratic effect, P < or = 0.025). The ability of macrophages to adhere to glass surfaces was impaired by increasing concentrations of T-2 Tetraol (linear effect, P < or = 0.003). This experiment demonstrates that T-2 Tetraol is cytotoxic to chicken macrophages in vitro.

Differential association of T-2 and T-2 Tetraol with mammalian cells

J Pharmacol Exp Ther 1989 Sep;250(3):860-6.PMID:2778715doi

The interactions of T-2 and its metabolite T-2 Tetraol (hereafter tetraol) with CHO (Chinese hamster ovary cells) and CHO ribosomes were studied. T-2 was about 300-fold more potent at inhibiting protein synthesis in CHO than was tetraol. Association of T-2 with CHO was highly specific and achieved a maximum at a concentration producing complete inhibition of protein synthesis. Association of tetraol with CHO was of low specificity, but the specific fraction did correlate with the dose-response curve for protein synthesis inhibition. Binding of both T-2 and tetraol to isolated CHO ribosomes was quantitatively similar and highly specific. With isolated ribosomes, each toxin competed effectively for the binding of the other. Using intact cells, tetraol competed for T-2 cell association, but not the converse. The kinetics at physiological temperature for total and specific T-2 cell association were much more rapid than those for tetraol. Furthermore, the rate of tetraol-cell association was indistinguishable from the rate for cellular uptake of tritiated water. At 0 degrees C, there was a substantial association of T-2 with cells, whereas none was observed with tetraol. The kinetics of dissociation of both toxins from CHO were similar. We conclude that T-2 rapidly crosses the cell membrane of cells and binds to the intracellular target, the ribosomes. In contrast, tetraol is taken up by the cell much more slowly, and many more toxin molecules are found in the cell than there are ribosomes. It would appear that the main physical property of the toxins that brings about these results is the relative hydrophobicities of the molecules.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Appl Environ Microbiol 1987 Jan;53(1):17-21.PMID:3827243DOI:10.1128/aem.53.1.17-21.1987.

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.