Triadimefon
(Synonyms: 三唑酮) 目录号 : GC45078
A triazole fungicide
Cas No.:43121-43-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Triadimefon is a triazole fungicide used to control powdery mildew, rusts, and other fungal pests on grains, fruit and vegetable crops, turf, shrubs, and trees. It inhibits lanosterol 14α-demethylase, interfering with oxidative demethylation reactions in the ergosterol biosynthesis pathway of fungi, and also blocks gibberellin biosynthesis.
| Cas No. | 43121-43-3 | SDF | |
| 别名 | 三唑酮 | ||
| Canonical SMILES | ClC1=CC=C(OC(N2C=NC=N2)C(C(C)(C)C)=O)C=C1 | ||
| 分子式 | C14H16ClN3O2 | 分子量 | 293.8 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS(pH7.2) (1:1): 0.5 mg/ml,Ethanol: 10 mg/ml | 储存条件 | Store at -20°C |
| 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 | 3.4037 mL | 17.0184 mL | 34.0368 mL |
| 5 mM | 0.6807 mL | 3.4037 mL | 6.8074 mL |
| 10 mM | 0.3404 mL | 1.7018 mL | 3.4037 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。
Effect of Triadimefon on rat placental morphology, function, and gene expression
Toxicol Lett 2022 Sep 27;371:25-37.PMID:36179991DOI:10.1016/j.toxlet.2022.09.009.
Triadimefon is a fungicide that is broadly used to treat fungal diseases of plants. It causes developmental toxicity in the animal model. Whether Triadimefon disrupts the placental function and the underlying mechanism remains unclear. Thirty-six female pregnant Sprague-Dawley rats were randomly assigned into four groups and were orally administered via gavage of Triadimefon (0, 25, 50, and 100 mg/kg/day) for 10 days from gestational day (GD) 12-21. Triadimefon disrupted the structure of the placenta, leading to hypertrophy, abnormal hemodynamics, including fibrin exudation, edema, hemorrhage, infarction, and inflammation. RNA-seq analysis showed that Triadimefon down-regulated the expression of developmental and metabolic genes, while up-regulating the immune/inflammatory genes. The qPCR showed that Triadimefon markedly down-regulated the expression of Cpt1c, Scd2, Ldlr, Dvl1, Flt4, and Vwf and their proteins, while up-regulating the expression of Cyp1a1, Star, Ccl5, and Cx3cr1 and their proteins at 25-100 mg/kg. Western blot showed that Triadimefon reduced the level of STAT3 at doses of 50 and 100 mg/kg and the phosphorylation of AMPK at 100 mg/kg. In conclusion, Triadimefon severely damages the structure and function of the placenta, leading to placental hypertrophy, local blood circulation disorders, and inflammation and this may be associated with its down-regulation of genes related to metabolism and nutrient transport and the up-regulation of inflammatory genes via STAT3 and AMPK signals.
Triadimefon suppresses fetal adrenal gland development after in utero exposure
Toxicology 2021 Oct;462:152932.PMID:34508824DOI:10.1016/j.tox.2021.152932.
Triadimefon is a broad-spectrum antifungal agent, which is widely used in agriculture to control mold and fungal infections. It is considered an endocrine disruptor. Whether Triadimefon exposure can inhibit the development of fetal adrenal glands and the underlying mechanism remain unclear. Thirty-two pregnant female Sprague-Dawley rats were randomly divided into four groups. Dams were gavaged Triadimefon (0, 25, 50, and 100 mg/kg/day) daily for 10 days from gestational day (GD) 12 to GD 21. Triadimefon significantly reduced the thickness of the zona fasciculata of male fetuses at 100 mg/kg, although it did not change the thickness of the zona glomerulosa. It significantly reduced the serum aldosterone levels of male fetuses at a dose of 100 mg/kg, and significantly reduced serum corticosterone and adrenocorticotropic hormone levels at doses of 50 and 100 mg/kg. Triadimefon significantly down-regulated the expression of Agtr1, Mc2r, Star, Cyp11b1, Cyp11b2, Igf1, Nr5a1, Sod2, Gpx1, and Cat, but did not affect the mRNA levels of Scarb1, Cyp11a1, Cyp21, Hsd3b1, and Hsd11b2. Triadimefon markedly reduced AT1R, CYP11B2, IGF1, NR5A1, and MC2R protein levels. Triadimefon significantly reduced the phosphorylation of AKT1 and ERK1/2 at 100 mg/kg without affecting the phosphorylation of AKT2. In contrast, it significantly increased AMPK phosphorylation at 100 mg/kg. In conclusion, exposure to Triadimefon during gestation inhibits the development of fetal adrenal cortex in male fetuses. This inhibition is possibly due to the reduction of several proteins required for the synthesis of steroid hormones, and may be involved in changes in antioxidant contents and the phosphorylation of AKT1, ERK1/2, and AMPK.
Enantioselective metabolism of Triadimefon and its chiral metabolite triadimenol in lizards
Ecotoxicol Environ Saf 2017 Sep;143:159-165.PMID:28535441DOI:10.1016/j.ecoenv.2017.05.024.
Chinese lizards (Eremias argus) were exposed to separated R-(-)-triadimefon, S-(+)-triadimefon and racemic Triadimefon to evaluate enantioselective accumulation of Triadimefon. After single oral administration of R-(-)-triadimefon, S-(+)-triadimefon and racemic Triadimefon, the time-concentration curves in different tissues were found to be different. Triadimefon enantiomers crossed the blood-brain barrier and brain is a main target organ. The residues of Triadimefon enantiomers in fat were highest after 24h indicating that fat was the main tissue of accumulation. In racemic Triadimefon exposure group, the enantiomer fractions of R-(-)-triadimefon in different tissues showed that the differences between R-(-)-triadimefon and S-(+)-triadimefon were significant in absorption and metabolism, but the differences became smaller in exclusion and accumulation. From the results of mathematical models, S-(+)-triadimefon was absorbed and eliminated faster than R-(-)-triadimefon, and R-(-)-triadimefon was easily distributed in the tissues and more easily converted into its metabolites. Furthermore, among the four enantiomers of triadimenol, SR-(-)-triadimenol produced by S-(+)-triadimefon may have the highest fungicidal activity and the strongest biological toxicity, RR-(+)-triadimenol produced by R-(-)-triadimefon was most likely to bioaccumulate in lizard. Identifying toxicological effects and dose-response relationship of SR-(-)-triadimenol and RR-(+)-triadimenol will help fully assess the risk of TF enantiomers use in the future. The results enrich and supplement the knowledge of the environmental fate of Triadimefon enantiomers.
Uptake and translocation of Triadimefon by wheat (Triticum aestivum L.) grown in hydroponics and soil conditions
J Hazard Mater 2022 Feb 5;423(Pt A):127011.PMID:34461532DOI:10.1016/j.jhazmat.2021.127011.
Residual pesticides in soil may be taken in by plants and thus have a risk for plant growth and food safety. In this study, uptake of Triadimefon and its subsequent translocation and accumulation were investigated with wheat as model plants. The results from hydroponics indicated that Triadimefon was absorbed by wheat roots mainly through apoplastic pathway and predominantly distributed into the water soluble fractions (66.7-76.0%). After being uptaken by roots, Triadimefon was easily translocated upward to wheat shoots and leaves. Interestingly, Triadimefon in leaves was mainly distributed in the soluble fraction by 52.5% at the beginning, and gradually transferred into the cell wall by 47.2% at equilibrium. The uptake of Triadimefon from soils by wheat plants was similar to that in hydroponics. Its accumulation were mainly governed by adsorption of the fungicide onto soils, and positively correlated with its concentration in in situ pore water (CIPW). Thus, CIPW can be suitable for predicting the uptake of Triadimefon by wheat from soils. Accordingly, uptake of Triadimefon by wheat was predicted well by using the partition-limited model. Our study provides valuable information for guiding the practical application and safety evaluation of Triadimefon.
Triadimefon increases fetal Leydig cell proliferation but inhibits its differentiation of male fetuses after gestational exposure
Ecotoxicol Environ Saf 2021 Oct 30;228:112942.PMID:34737156DOI:10.1016/j.ecoenv.2021.112942.
Triadimefon is a broad-spectrum fungicide widely applied in the agriculture. It is believed to be an endocrine disruptor. Whether Triadimefon can inhibit the development of fetal Leydig cells and the underlying mechanisms are unknown. Thirty-two female pregnant Sprague-Dawley rats were randomly assigned into four groups and were dosed via gavage of Triadimefon (0, 25, 50, and 100 mg/kg/day) for 9 days from gestational day (GD) 12-20. Triadimefon significantly reduced serum testosterone level in male fetuses at 100 mg/kg. The double immunofluorescence staining of proliferating cell nuclear antigen (PCNA) and cytochrome P450 cholesterol side-chain cleavage (a biomarker for fetal Leydig cells) was used to measure PCNA-labeling in fetal Leydig cells. It markedly increased fetal Leydig cell number primarily via increasing single cell population and elevated the PCNA-labeling of fetal Leydig cells in male fetuses at 100 mg/kg while it induced abnormal aggregation of fetal Leydig cells. The expression levels of fetal Leydig cell genes, Lhcgr, Scarb1, Star, Cyp11a1, Hsd3b1, Cyp17a1, Hsd17b3, Insl3 and Nr5a1, were determined to explore its effects on fetal Leydig cell development. We found that Triadimefon markedly down-regulated the expression of Leydig cell genes, Hsd17b3, Insl3, and Nr5a1 as low as 25 mg/kg and Scarb1 and Cyp11a1 at 100 mg/kg. It did not affect Sertoli cell number but markedly down-regulated the expression of Sertoli cell gene Amh at 50 and 100 mg/kg. Triadimefon significantly down-regulated the expression of antioxidant genes Sod1, Gpx1, and Cat at 25-100 mg/kg, suggesting that it can induce oxidative stress in fetal testis, and it reduced the phosphorylation of ERK1/2 and AKT2 at 100 mg/kg, indicating that it can inhibit the development of fetal Leydig cells. In conclusion, gestational exposure to Triadimefon inhibits the development of fetal Leydig cells in male fetuses by inhibiting its differentiation.