Difenoconazole
(Synonyms: 苯醚甲环唑) 目录号 : GC47217
A triazole fungicide
Cas No.:119446-68-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >96.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Difenoconazole is a broad-spectrum triazole fungicide that inhibits ergosterol biosynthesis via inhibition of the cytochrome P450-dependent 14α-demethylation of lanosterol, which results in disruption of the fungal cell membrane and cell death.1,2 It inhibits the growth of F. graminearum isolates in vitro (EC50s = 1.69-19.6 mg/L for mycelial growth).2 It also inhibits growth of A. sonali, F. fulva, B. cinerea, and R. solani (EC50s = 0.131, 0.069, 0.297, and 0.252 mg/L, respectively).3 Difenoconazole reduces germtube growth of A. caricae, the mold responsible for black spot in papaya plants (EC50 = 2 ppm).4 It exhibits acute aquatic toxicity, reducing growth of S. obliquus algae (EC50 = 1.338 μg/ml) and decreasing survival of D. magna (LD50 = 0.298 μg/ml).3 Difenoconazole is also lethal to zebrafish (D. rerio) embryos, larvae, and adults (LC50s = 2.34, 1.17, and 1.45 mg/L, respectively).5 At sub-LC50 concentrations, difenoconazole induces pericardial and yolk sac edema in zebrafish embryos, body blackening and slowed heart rate in larvae, and decreased body weight and length in adults.
1.Zarn, J.A., BrÜschweiler, B.J., and Schlatter, J.R.Azole fungicides affect mammalian steroidogenesis by inhibiting sterol 14 α-demethylase and aromataseEnviron. Health Perspect.111(3)255-261(2003) 2.Rekanovi?, E., Mihajlovi?, M., and Poto?nik, I.In vitro sensitivity of Fusarium graminearum (schwabe) to difenoconazole, prothioconazole and thiophanate-methylPestic. Phytomed.25(4)325-333(2010) 3.Dong, F., Li, J., Chankvetadze, B., et al.Chiral triazole fungicide difenoconazole: Absolute stereochemistry, stereoselective bioactivity, aquatic toxicity, and environmental behavior in vegetables and soilEnviron. Sci. Technol.47(7)3386-3394(2013) 4.Vawdrey, L.L., Grice, K.R.E., and Westerhuis, D.Field and laboratory evaluations of fungicides for the control of brown spot (Corynespora cassiicola) and black spot (Asperisporium caricae) of papaya in far north Queensland, AustraliaAus. Plant Path.37(6)552-558(2008) 5.Mu, X., Pang, S., Sun, X., et al.Evaluation of acute and developmental effects of difenoconazole via multiple stage zebrafish assaysEnviron. Pollut.175(2013)147-157(2013)
| Cas No. | 119446-68-3 | SDF | |
| 别名 | 苯醚甲环唑 | ||
| Canonical SMILES | ClC1=CC=C(OC2=CC(Cl)=C(C3(CN4C=NC=N4)OC(C)CO3)C=C2)C=C1 | ||
| 分子式 | C19H17Cl2N3O3 | 分子量 | 406.3 |
| 溶解度 | Chloroform: Slightly Soluble,Methanol: Slightly Soluble | 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 | 2.4612 mL | 12.3062 mL | 24.6124 mL |
| 5 mM | 0.4922 mL | 2.4612 mL | 4.9225 mL |
| 10 mM | 0.2461 mL | 1.2306 mL | 2.4612 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。
Metagenomic ecotoxicity assessment of trace Difenoconazole on freshwater microbial community
Chemosphere 2022 May;294:133742.PMID:35090847DOI:10.1016/j.chemosphere.2022.133742.
Difenoconazole, a typical triazole fungicide, inhibits the activity of cytochrome P450 enzyme in fungi, and is extensively used in protecting fruits, vegetables, and cereal crops. However, reports elucidating the effects of Difenoconazole on aquatic microbial communities are limited. Our study showed that Difenoconazole promoted microalgae growth at concentrations ranging from 0.1 to 5 μg/L, which was similar with its environmental residual concentrations. Metagenomic analysis revealed that the aquatic microbial structure could self-regulate to cope with difenoconazole-induced stress by accumulating bacteria exhibiting pollutant degrading abilities. In the short-term, several functional pathways related to xenobiotic biodegradation and analysis were upregulated to provide ability for aquatic microbial community to process xenobiotic stress. Moreover, most disturbed ecological functions were recovered due to the redundancy of microbial communities after prolonged exposure. Furthermore, the risks associated with the dissemination of antibiotic resistance genes were enhanced by Difenoconazole in the short-term. Overall, our study contributes to a comprehensive understanding of the difenoconazole-induced ecological impacts and the behavior of aquatic microbial communities that are coping with xenobiotic stress.
Difenoconazole causes cardiotoxicity in common carp (Cyprinus carpio): Involvement of oxidative stress, inflammation, apoptosis and autophagy
Chemosphere 2022 Nov;306:135562.PMID:35792209DOI:10.1016/j.chemosphere.2022.135562.
Difenoconazole, a commonly used broad-spectrum triazole fungicide, is widely applied to fish culture in paddy fields. Due to its high chemical stability, low biodegradability, and easy transfer, Difenoconazole persists in aquatic systems, raising public awareness of environmental threats. Difenoconazole causes cardiotoxicity in carp, however, the potential mechanisms of difenoconazole-induced cardiotoxicity remain unclear. Here, common carp were exposed to Difenoconazole, and cardiotoxicity was evaluated by measuring the creatine kinase (CK) and the lactate dehydrogenase (LDH) in the serum. Cardiac pathological injury was determined by HE staining. The content and expression of oxidative stress indicators were detected using biochemical kits and qPCR analysis. Changes in inflammation-related cytokines were examined by qPCR. Apoptosis levels were assessed by TUNEL assay and qPCR. The occurrence of autophagy was measured by western blotting detection of autophagy flux LC3II/LC3I, and autophagy regulatory pathways were detected using qPCR. The results showed that Difenoconazole exposure induced cardiotoxicity accompanied by obviously elevated LDH and CK levels and caused myocardial fibers to swell and inflammatory cells to increase. Elevated peroxide MDA and reduced transcriptional and activity levels of the antioxidant enzymes CAT, SOD and GSH-Px were dependent on the Nrf2/Keap-1 pathway. Moreover, the proinflammatory cytokines IL-1β, IL-6, and TNF-α were upregulated, iNOS activity was enhanced, whereas the anti-inflammatory cytokines TGF-β1 and IL-10 were downregulated after exposure to Difenoconazole. Moreover, apoptosis was observed in the TUNEL assay and mediated through the p53/Bcl-2/Bax-Caspase-9 mitochondrial pathway. Furthermore, Difenoconazole increased the autophagy markers LC3II, ATG5 and p62 and regulated them through the PI3K/AKT/mTOR pathway. Altogether, this study demonstrated that Difenoconazole exposure caused common carp cardiotoxicity, which is regulated by oxidative stress, inflammation, apoptosis and autophagy, providing central data for toxicological risk assessment of Difenoconazole in the ecological environment.
Difenoconazole induces oxidative DNA damage and mitochondria mediated apoptosis in SH-SY5Y cells
Chemosphere 2021 Nov;283:131160.PMID:34139443DOI:10.1016/j.chemosphere.2021.131160.
Difenoconazole is one of the most typical triazole fungicides. Difenoconazole is widely used in the field of agricultural production, and its health and safety problems need to be further studied. The main purpose of this paper is to verify the neurotoxicity of Difenoconazole at the cellular level. In this study, SH-SY5Y cell line of human neuroblastoma was used to evaluate its potentially toxic effects and molecular mechanism in vitro. The research indicated that Difenoconazole could reduce cell viability and inhibit cell proliferation, induce DNA damage and accelerate programmed cell death. Further studies showed that Difenoconazole induced DNA double-strand breaks, intracellular generation of ROS, cleaved PARP, mitochondrial membrane potential collapse, induced Cyt c release, and Bax/Bcl-2 ratio increase in SH-SY5Y cells. In conclusion, the cytotoxicity of Difenoconazole revealed its toxic effect on SH-SY5Y cells, and the IC50 value was 55.41 μM after 24 h exposure. Meanwhile, the genetic toxicity of Difenoconazole has revealed that it can induce DNA damage and apoptosis of SH-SY5Y cells. Through this study, the toxic effects of Difenoconazole on SH-SY5Y cells are further understood, which provides a more scientific basis for its safe use and risk control.
Sub-Chronic Difenoconazole Exposure Induced Gut Microbiota Dysbiosis in Mice
Toxics 2022 Jan 12;10(1):34.PMID:35051076DOI:10.3390/toxics10010034.
Difenoconazole (DIF) is a widely separated triazole fungicide in many countries. The excessive usage of DIF increases the high volume of residues in agriculture production and water bodies. Some previous studies demonstrated the toxic effects of DIF on non-target animals, however, there were still some gaps in the knowledge of the potential hazards of DIF to mammals and human health. Herein, 7-week-old male mice were exposed to 30 and 100 mg/kg/day DIF for 14 and 56 days. We observed that 56 days of DIF exposure decreased the colonic mucus expression of alcin blue-periodic acid-schiff (AB-PAS) stain and the immunochemical stain of muc2 protein. The transcript levels of mucin protein (muc1, muc2 and muc3) decreased significantly in the gut of mice followed 56 days of 100 mg/kg/day DIF exposure. In addition, the gut microbiota composition was also affected after 14 or 56 days of DIF exposure. Although the mucus expression after 14 days of DIF exposure only decreased slightly, the gut microbiota composition compared with the control group was changed significantly. Moreover, the DIF-30 and DIF-100 caused respectively different changes on the gut microbiota. The relative abundance of Bacteroidetes decreased significantly after 14 days and 56 days of DIF exposure. After 14 days of DIF exposure, there were 35 and 18 differential genera in the DIF-30 and DIF-100 group, respectively. There were 25 and 32 differential genera in the DIF-30 and DIF-100 group after 56 days of exposure, respectively. Meanwhile, the alpha diversity indexes, including observed species, Shannon, Simpson, Chao1 and ACE, in gut microbiota decreased significantly after 56 days of DIF exposure. Interestingly, the relative abundance of Akkermansia increased significantly after 56 days of 100 mg/kg/d DIF exposure. Although Akkermansia was considered as one probiotic, the phenomenon of dramatic Akkermansia increase with the decrease in gut microbiota diversity needed further discussion. These results provided some new insights on how DIF exposure impacts the mucus barrier and induces gut microbiota dysbiosis.
Uptake and distribution of Difenoconazole in rice plants under different culture patterns
Food Addit Contam Part A Chem Anal Control Expo Risk Assess 2022 Jun;39(6):1100-1108.PMID:35357266DOI:10.1080/19440049.2022.2056640.
The effects of spraying and root irrigation on the uptake and transport of the fungicide Difenoconazole under hydroponic and soil cultivation were investigated. Rice was used as the crop for a short-term exposure experiment. A modified QuEChERS pre-treatment combined with ultra-high-performance liquid chromatography-tandem mass spectrometry was used to extract and detect Difenoconazole from rice plants, water and soil. The recoveries of Difenoconazole were in the range of 72.8-110.5%, with a relative standard deviation of 2.4-19.5% for all the samples when spiked with 0.01, 0.1 and 1 mg kg-1 of Difenoconazole, respectively. The limit of quantitation (LOQ) of this method was 0.01 mg kg-1. The exposure results showed that Difenoconazole could be absorbed by rice plants and transmitted to different parts of rice plants in all the treatments. In the hydroponic experiment, Difenoconazole was mainly distributed in the roots of rice regardless of whether irrigation or spraying was used. For rice cultivated in soil, Difenoconazole mainly accumulated in leaves after the root irrigation treatment, whereas after the spraying treatment, the rice roots were the main site of accumulation of Difenoconazole. This experiment extends our knowledge of the influence of the cultivation system and application mode on the translocation of Difenoconazole in rice plants.