T-2 Toxin
(Synonyms: T-2毒素(镰刀菌属),T-2 Mycotoxin) 目录号 : GC44981
A trichothecene mycotoxin
Cas No.:21259-20-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
T-2 Toxin (T-2 Mycotoxin) is a toxic trichothecene mycotoxin produced by various Fusarium species in feedstuffs and cereal grains, LD50 values of T-2 Toxin in mice and rats are 5.2 and 1.5 mg/kg BWa,respectively [1]. T-2 Toxin (T-2 Mycotoxin) can be transformed into a variety of metabolite, the typical metabolites of T-2 toxin in animals are HT-2 toxin and T-2-triol, which are hydrolysates[1]. T-2 Toxin (T-2 Mycotoxin) is an inhibitor of protein synthesis resulting from binding peptidyltransferase, which is an integral part of the 60s ribosomal subunit. T-2 Toxin (T-2 Mycotoxin) inhibits the synthesis of DNA and RNA, interferes with the metabolism of membrane phospholipids, and increases the level of liver lipid peroxides[1]. T-2 Toxin (T-2 Mycotoxin) induces apoptosis in the immune system, gastrointestinal tissues, and fetal tissues[2].
References:
[1]. Li Y, et al. T-2 toxin, a trichothecene mycotoxin: review of toxicity, metabolism, and analytical methods. J Agric Food Chem. 2011 Apr 27;59(8):3441-53.
[2]. .Sun YX, et al. Toxicokinetics of T-2 toxin and its major metabolites in broiler chickens after intravenous and oral administration. J Vet Pharmacol Ther. 2015 Feb;38(1):80-5
| Cas No. | 21259-20-1 | SDF | |
| 别名 | T-2毒素(镰刀菌属),T-2 Mycotoxin | ||
| Canonical SMILES | CC1=C[C@]2([H])[C@]([C@]3(C)[C@@]4(OC4)[C@]([C@H](O)[C@H]3OC(C)=O)([H])O2)(COC(C)=O)C[C@@H]1OC(CC(C)C)=O | ||
| 分子式 | C24H34O9 | 分子量 | 466.6 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS(pH7.2) (1:1): 0.5 mg/ml,Ethanol: 20 mg/ml | 储存条件 | Store at -20°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.1432 mL | 10.7158 mL | 21.4316 mL |
| 5 mM | 0.4286 mL | 2.1432 mL | 4.2863 mL |
| 10 mM | 0.2143 mL | 1.0716 mL | 2.1432 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
T-2 Toxin-The Most Toxic Trichothecene Mycotoxin: Metabolism, Toxicity, and Decontamination Strategies
Molecules 2021 Nov 14;26(22):6868.PMID:34833960DOI:10.3390/molecules26226868.
Among trichothecenes, T-2 Toxin is the most toxic fungal secondary metabolite produced by different Fusarium species. Moreover, T-2 is the most common cause of poisoning that results from the consumption of contaminated cereal-based food and feed reported among humans and animals. The food and feed most contaminated with T-2 Toxin is made from wheat, barley, rye, oats, and maize. After exposition or ingestion, T-2 is immediately absorbed from the alimentary tract or through the respiratory mucosal membranes and transported to the liver as a primary organ responsible for toxin's metabolism. Depending on the age, way of exposure, and dosage, intoxication manifests by vomiting, feed refusal, stomach necrosis, and skin irritation, which is rarely observed in case of mycotoxins intoxication. In order to eliminate T-2 Toxin, various decontamination techniques have been found to mitigate the concentration of T-2 Toxin in agricultural commodities. However, it is believed that 100% degradation of this toxin could be not possible. In this review, T-2 Toxin toxicity, metabolism, and decontamination strategies are presented and discussed.
T-2 Toxin causes dysfunction of Sertoli cells by inducing oxidative stress
Ecotoxicol Environ Saf 2021 Dec 1;225:112702.PMID:34478974DOI:10.1016/j.ecoenv.2021.112702.
T-2 Toxin is an inevitable mycotoxin in food products and feeds. It is a proven toxicant impairing the male reproductive system. However, previous studies have concentrated on the toxic effect of T-2 Toxin on Leydig cells, with little attention on the Sertoli cell cytotoxicity. Therefore, this study aimed to establish the toxic mechanism of T-2 Toxin on Sertoli cells. The Sertoli cell line (TM4 cell) was cultured and exposed to different concentrations of T-2 Toxin with/without N-acetyl-L-cysteine (NAC) for 24 h. A CCK-8 assay then measured the cell viability. In addition, the expression of TM4 cell biomarkers (FSHR and ABP) and functional factors (occludin (Ocln), zonula occluden-1 (ZO-1), Connexin 43 (Cx-43), and N-Cadherin (N-cad)) were measured by qRT-PCR and Western blotting. The oxidative stress status (ROS, MDA, CAT, and SOD) and apoptosis rate, including the caspase-9, 8, and 3 activities in TM4 cells, were analyzed. We established that (1): T-2 Toxin decreased TM4 cells viability and the half-maximal inhibitory concentration was 8.10 nM. (2): T-2 toxin-induced oxidative stress, evidenced by increased ROS and MDA contents, and inhibited CAT and SOD activities. (3): T-2 Toxin inhibited FSHR, ABP, ocln, ZO-1, Cx-43, and N-Cad expressions. (4): T-2 Toxin promoted TM4 cell apoptosis and caspase-9, 8, and 3 activities. (5): N-acetyl-L-cysteine relieved oxidative stress, functional impairment, and apoptosis in TM4 cells treated with T-2 Toxin. Thus, T-2 Toxin induced TM4 cell dysfunction through ROS-induced apoptosis.
T-2 Toxin and its cardiotoxicity: New insights on the molecular mechanisms and therapeutic implications
Food Chem Toxicol 2022 Sep;167:113262.PMID:35792220DOI:10.1016/j.fct.2022.113262.
T-2 Toxin is one of the most toxic and common trichothecene mycotoxins, and can cause various cardiovascular diseases. In this review, we summarized the current knowledge-base and challenges as it relates to T-2 Toxin related cardiotoxicity. The molecular mechanisms and potential treatment approaches were also discussed. Pathologically, T-2 toxin-induced cardiac toxicity is characterized by cell injury and death in cardiomyocyte, increased capillary permeability, necrosis of cardiomyocyte, hemorrhage, and the infiltration of inflammatory cells in the heart. T-2 Toxin exposure can cause cardiac fibrosis and finally lead to cardiac dysfunction. Mechanistically, T-2 Toxin exposure-induced cardiac damage involves the production of ROS, mitochondrial dysfunction, peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling pathway, endoplasmic reticulum (ER stress), transforming growth factor beta 1 (TGF-β1)/smad family member 2/3 (Smad2/3) signaling pathway, and autophagy and inflammatory responses. Antioxidant supplementation (e.g., catalase, vitamin C, and selenium), induction of autophagy (e.g., rapamycin), blockade of inflammatory signaling (e.g., methylprednisolone) or treatment with PPAR-γ agonists (e.g., pioglitazone) may provide protective effects against these detrimental cardiac effects caused by T-2 Toxin. We believe that our review provides new insights in understanding T-2 Toxin exposure-induced cardiotoxicity and fuels effective prevention and treatment strategies against this important food-borne toxin-induced health problems.
Toxicity and detoxification of T-2 Toxin in poultry
Food Chem Toxicol 2022 Nov;169:113392.PMID:36044934DOI:10.1016/j.fct.2022.113392.
This review summarizes the updated knowledge on the toxicity of T-2 on poultry, followed by potential strategies for detoxification of T-2 in poultry diet. The toxic effects of T-2 on poultry include cytotoxicity, genotoxicity, metabolism modulation, immunotoxicity, hepatotoxicity, gastrointestinal toxicity, skeletal toxicity, nephrotoxicity, reproductive toxicity, neurotoxicity, etc. Cytotoxicity is the primary toxicity of T-2, characterized by inhibiting protein and nucleic acid synthesis, altering the cell cycle, inducing oxidative stress, apoptosis and necrosis, which lead to damages of immune organs, liver, digestive tract, bone, kidney, etc., resulting in pathological changes and impaired physiological functions of these organs. Glutathione redox system, superoxide dismutase, catalase and autophagy are protective mechanisms against oxidative stress and apoptosis, and can compensate the pathological changes and physiological functions impaired by T-2 to some degree. T-2 detoxifying agents for poultry feeds include adsorbing agents (e.g., aluminosilicate-based clays and microbial cell wall), biotransforming agents (e.g., Eubacterium sp. BBSH 797 strain), and indirect detoxifying agents (e.g., plant-derived antioxidants). These T-2 detoxifying agents could alleviate different pathological changes to different degrees, and multi-component T-2 detoxifying agents can likely provide more comprehensive protection against the toxicity of T-2.
Review of the Reproductive Toxicity of T-2 Toxin
J Agric Food Chem 2020 Jan 22;68(3):727-734.PMID:31895560DOI:10.1021/acs.jafc.9b07880.
T-2 Toxin, an inevitable environmental pollutant, is the most toxic type A trichothecene mycotoxin. Reproductive disruption is a key adverse effect of T-2 Toxin. Herein, this paper reviews the reproductive toxicity of T-2 Toxin and its mechanisms in male and female members of different species. The reproductive toxicity of T-2 Toxin is evidenced by decreased fertility, disrupted structures and functions of reproductive organs, and loss of gametogenesis in males and females. T-2 Toxin disrupts the reproductive endocrine axis and inhibits reproductive hormone synthesis. Furthermore, exposure to T-2 Toxin during pregnancy results in embryotoxicity and the abnormal development of offspring. We also summarize the research progress in counteracting the reproductive toxicity of T-2 Toxin. This review provides information toward a comprehensive understanding of the reproductive toxicity mechanisms of T-2 Toxin.