T-2 Toxin
(Synonyms: T-2毒素(镰刀菌属),T-2 Mycotoxin) 目录号 : GC44981
T-2 Toxin是最常见且毒性最强的单端孢霉烯类霉菌毒素之一，主要由镰刀菌属在谷物和饲料中产生。T-2 Toxin是一种A类非大环三萜毒素，其毒性机制是通过结合肽转移酶来抑制蛋白质合成。
Cas No.:21259-20-1
Sample solution is provided at 25 µL, 10mM.
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T-2 Toxin is one of the most common and potent trichothecene mycotoxins, primarily produced by Fusarium species in grains and animal feed[1]. T-2 Toxin is a type A non-macrocyclic trichothecene toxin, and its toxic mechanism involves inhibiting protein synthesis by binding to peptidyl transferase[2]. T-2 Toxin can be metabolized in animals into hydrolysis products such as HT-2 Toxin and T-2 triol[3]. T-2 Toxin can cross the blood-brain barrier and accumulate in the central nervous system, thus producing significant neurotoxicity[4].
In vitro, treatment of neonatal rat primary cardiomyocytes with T-2 Toxin (0.25-1µM) for 24h induced cardiomyocyte damage and inhibited cell viability in a dose-dependent manner[5]. Treatment of rat ovarian granulosa cells with T-2 Toxin (1-100nM) for 24h inhibited cell growth, induced apoptosis, led to ROS accumulation, and decreased mitochondrial membrane potential in a dose-dependent manner[6].
In vivo, treatment of mice with T-2 Toxin (5.94mg/kg) via transdermal administration or T-2 Toxin (1.57mg/kg) via subcutaneous injection for 0-7 days both increased reactive oxygen species production, glutathione depletion, lipid peroxidation, and protein carbonyl content in mouse brain tissue in a time-dependent manner. Transdermal administration significantly increased the expression of superoxide dismutase and catalase, while subcutaneous administration significantly increased the expression of glutathione reductase and glutathione peroxidase[7].
References:
[1] Janik E, Niemcewicz M, Podogrocki M, et al. T-2 Toxin—The most toxic trichothecene mycotoxin: Metabolism, toxicity, and decontamination strategies[J]. Molecules, 2021, 26(22): 6868.
[2] Meneely J, Greer B, Kolawole O, et al. T-2 and HT-2 Toxins: toxicity, occurrence and analysis: a review[J]. Toxins, 2023, 15(8): 481.
[3] Li Y, Wang Z, Beier R C, et al. T-2 Toxin, a trichothecene mycotoxin: review of toxicity, metabolism, and analytical methods[J]. Journal of agricultural and food chemistry, 2011, 59(8): 3441-3453.
[4] Wang Y, Wang B, Wang P, et al. Review of neurotoxicity of T-2 Toxin[J]. Mycotoxin research, 2024, 40(1): 85-95.
[5] Xu J, Pan S, Gan F, et al. Selenium deficiency aggravates T-2 Toxin-induced injury of primary neonatal rat cardiomyocytes through ER stress[J]. Chemico-biological interactions, 2018, 285: 96-105.
[6] Wu J, Jing L, Yuan H, et al. T-2 Toxin induces apoptosis in ovarian granulosa cells of rats through reactive oxygen species-mediated mitochondrial pathway[J]. Toxicology letters, 2011, 202(3): 168-177.
[7] Chaudhary M, Rao P V L. Brain oxidative stress after dermal and subcutaneous exposure of T-2 Toxin in mice[J]. Food and Chemical Toxicology, 2010, 48(12): 3436-3442.
T-2 Toxin是最常见且毒性最强的单端孢霉烯类霉菌毒素之一，主要由镰刀菌属在谷物和饲料中产生[1]。T-2 Toxin是一种A类非大环三萜毒素，其毒性机制是通过结合肽转移酶来抑制蛋白质合成[2]。T-2 Toxin可在动物体内代谢转化为HT-2毒素、T-2-三醇等水解产物[3]。T-2 Toxin能够穿过血脑屏障并在中枢神经系统蓄积，从而产生显著的神经毒性[4]。
在体外，T-2 Toxin（0.25-1µM）处理新生大鼠原代心肌细胞24h，以剂量依赖性方式诱导了心肌细胞损伤，抑制了细胞活力[5]。T-2 Toxin（1-100nM）处理大鼠卵巢颗粒细胞24h，以剂量依赖性方式抑制了细胞的生长，诱导了细胞凋亡，导致细胞中ROS积累，降低了线粒体膜电位[6]。
在体内，T-2 Toxin（5.94mg/kg）通过经皮给药或者T-2 Toxin（1.57mg/kg）通过皮下注射给药处理小鼠0-7天，均以时间依赖性方式增加了小鼠脑组织中活性氧生成、谷胱甘肽消耗、脂质过氧化和蛋白质羰基含量，经皮给药途径中超氧化物歧化酶和过氧化氢酶的表达显著增加，而皮下给药途径中谷胱甘肽还原酶和谷胱甘肽过氧化物酶的表达显著增加[7]。
| Cell experiment [1]: | |
Cell lines | Cardiomyocytes |
Preparation Method | Cardiomyocytes were cultured in DMEM medium containing 2μM selenomethionine and then exposed to different concentrations of T-2 Toxin (0.125, 0.25, 0.5, 1μM) for 24h. Cells cultured in DMEM medium containing 2μM selenomethionine served as the control group. The effects of T-2 Toxin on cardiomyocyte viability and cell damage were assessed using MTT assay and LDH assay. |
Reaction Conditions | 0.125, 0.25, 0.5, 1μM; 24h |
Applications | The cell viability was remarkably inhibited, and cell damage was increased after treatment with 0.25, 0.5, 1μM of T-2 Toxin. |
| Animal experiment [2]: | |
Animal models | Swiss albino female mice |
Preparation Method | T-2 Toxin was dissolved in minimum amount of DMSO and diluted in PBS before use. The mice were housed four to a cage and allowed to acclimatize 7 days prior to dosing. A day before percutaneous exposure of T-2 Toxin, hair on the back of the animals was closely clipped using a pair of scissors. For percutaneous route (p.c.), the diluted toxin solution was smeared uniformly on the back of the animals on a circular area of 1.5cm diameter, using a gas tight syringe. Subcutaneous injection was given using the gas tight syringe on the back of the animals. For time course study, animals were divided into four groups of six animals each for each time point (0, 1, 3 and 7 days) of p.c. and s.c. route. The mice were kept in separate groups as 0 (control), 1, 3 and 7 days post-exposure. Mice were administered 1 LD50 of T-2 Toxin by either p.c. (5.94mg/kg body mass) or s.c. (1.57mg/kg body mass) route. Control mice received equal volume DMSO by respective routes. |
Dosage form | 5.94mg/kg、1.57mg/kg; 0, 1, 3, 7 days; p.c.、s.c. |
Applications | T-2 Toxin treated animals showed time dependent increase in reactive oxygen species generation, glutathione depletion, lipid peroxidation and protein carbonyl content in brain in both the routes of exposure. Gene expression profile of antioxidant enzymes showed significant increase in superoxide dismutase and catalase in percutaenous route and glutathione reducatse and glutathione peroxidase in subcutaneous route. Immunoblot analysis of antioxidant enzymes correlated with gene expression profile. |
References: | |
| 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 | 428.6 μL | 2.1432 mL | 4.2863 mL |
| 10 mM | 214.3 μL | 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。
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