Diuron
(Synonyms: 敌草隆) 目录号 : GC60142
An herbicide
Cas No.:330-54-1
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
Diuron is a phenylurea herbicide that inhibits photosynthesis by preventing the formation of ATP and NADH.1 It decreases total respiration in roots of wheat by 50% and ground respiration by 100% when used at a concentration of 25 nM/ml.2 Diuron (2,500 ppm, dietary) increases the incidence of urinary bladder urothelial carcinomas in male and female mice by 73 and 27%, respectively.1 It increases the production of reactive oxygen species (ROS) in MCF-7 human breast adenocarcinoma and BeWo human placental choriocarcinoma cells when used at a concentration of 200 ?M and reduces viability of BeWo, but not MCF-7, cells when used at concentrations of 50 and 200 ?M.3 Formulations containing diuron have been used to control broadleaf and grass weeds and as a biocidal antifouling agent.
1.Da Rocha, M.S., Arnold, L.L., De Oliveira, M.L., et al.Diuron-induced rat urinary bladder carcinogenesis: Mode of action and human relevance evaluations using the International Programme on Chemical Safety frameworkCrit. Rev. Toxicol.44(5)393-406(2014) 2.Lundeg?rdh, H.The influence of diuron [3-(3,4-dichlorophenyl)-1,1-dimethylurea] on the respiratory and photosynthetic systems of plantsProc. Natl. Acad. Sci. USA53(4)703-710(1965) 3.Huovinen, M., Loikkanen, J., Naarala, J., et al.Toxicity of diuron in human cancer cellsToxicol. In Vitro29(7)1577-1586(2015)
| Cas No. | 330-54-1 | SDF | |
| 别名 | 敌草隆 | ||
| Canonical SMILES | O=C(NC1=CC=C(Cl)C(Cl)=C1)N(C)C | ||
| 分子式 | C9H10Cl2N2O | 分子量 | 233.09 |
| 溶解度 | DMSO: 250 mg/mL (1072.55 mM) | 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 | 4.2902 mL | 21.4509 mL | 42.9019 mL |
| 5 mM | 0.858 mL | 4.2902 mL | 8.5804 mL |
| 10 mM | 0.429 mL | 2.1451 mL | 4.2902 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。
Molecular signatures associated with Diuron exposure on rat urothelial mitochondria
Toxicol Mech Methods 2022 Oct;32(8):628-635.PMID:35379061DOI:10.1080/15376516.2022.2062271.
Diuron, 3-(3,4-dichlorophenyl)-1,1-dimethylurea, is a worldwide used herbicide whose biotransformation gives rise to the metabolites, 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU) and 3,4-dichloroaniline (DCA). Previous studies indicate that Diuron and/or its metabolites are toxic to the bladder urothelium of the Wistar rats where, under certain conditions of exposure, they may induce successively urothelial cell degeneration, necrosis, hyperplasia and eventually tumors. The hypothesis was raised that the molecular initiating event (MIE) of this Adverse Outcome Pathway is the mitochondrial toxicity of those compounds. Therefore, this study aimed to investigate in vitro the metabolic alterations resulting from urothelial mitochondria isolated from male Wistar rats exposure to Diuron, DCPMU and DCA at 10 and 100 µM. A non-targeted metabolomic analysis using mass spectrometry showed discriminative clustering among groups and alterations in the intensity abundance of membrane-associated molecules phosphatidylcholine, phosphatidylinositol and phosphatidylserine, in addition to methylhexanoyl-CoA and, particularly for Diuron 100 µM, dehydro-L-gulonate, all of them involved in critical mitochondrial metabolism. Collectively, these data indicate the mitochondrial dysfunction as an MIE that triggers cellular damage and death observed in previous studies.
Diuron environmental levels effects on marine nematodes: Assessment of ecological indices, taxonomic diversity, and functional traits
Chemosphere 2022 Jan;287(Pt 3):132262.PMID:34543897DOI:10.1016/j.chemosphere.2021.132262.
Coastal marine systems are the most sensitive zones to emerging pollutants. The present study aims to investigate the effect of Diuron on the meiofaunal assemblages, collected from the Bizerte channel (Tunisia). Microcosm experiments were set up using four increasing Diuron concentrations [D1 (10 ng g-1 dry weight (DW)), D2 (50 ng g-1 DW), D3 (250 ng g-1 DW) and (1250 ng g-1 DW)] compared to non-contaminated sediments (controls) and all plots were incubated for 30 days. Our results show that Diuron-supplemented sediments provoked the significant decrease of meiofaunal abundance as well as a change in nematodes' diversity and structure composition. All univariate indices, as well as the cumulative k-dominance, were lower in the Diuron than the control plot. Additionally, the ordination of treatments according to the two-dimensional nMDS plots analysis showed a clear structural separation of the Diuron treated replicates from the controls based on the functional groups lists. These current data emphasize the utility of the use of biological traits in the detection of disturbances in the aquatic biotope.
Diuron sorption isotherms in freshwater biofilms
Sci Total Environ 2019 Feb 15;651(Pt 1):1219-1225.PMID:30360253DOI:10.1016/j.scitotenv.2018.09.286.
Biofilms are excellent bioindicators for water quality assessment because of their ability to integrate contamination, and their position at the base of the trophic chain in aquatic environments. Pesticides are ubiquitous in aquatic environments and can constantly interact with aquatic organisms, including those that make up biofilms, at fluctuating concentrations. The aim of this study was to describe pesticide behaviour in biofilms. Previous research highlighted that contaminant sorption was not always linear, but no study considered organic bioaccumulation isotherms and toxic impacts to biofilms concurrently. In order to characterize pesticide sorption isotherms in biofilms and the mechanisms involved in the uptake process, we simultaneously assessed bioaccumulation and toxic impact of Diuron (a photosynthesis inhibiting herbicide) at the water-biofilm concentrations equilibrium. Mature biofilms grown on glass slides during one month were subsequently exposed in channels to 7 increasing concentrations of Diuron from 1 to 500 μg·L-1, plus a control condition, for 2 h with a flow velocity of 2 cm·s-1. Then, a Langmuir isotherm equation was fitted to the bioaccumulation data, and an Emax model to toxic impact results. This study established that Diuron bioaccumulation in biofilm is nonlinear, and allowed to calculate the Langmuir constant and maximal concentration of Diuron potentially accumulated in biofilm (up to 17,771 μg·g-1). In turn, we found that photosynthetic inhibition followed classical dose-response patterns with Diuron concentrations in the water, and that EC50 could be established at 75 μg·L-1. A continuous diffusion phenomenon was thus demonstrated but it was not linearly correlated to bioaccumulation, highlighting complex uptake mechanisms operating within the matrix. The coupling of toxicokinetic and toxicodynamic approaches provided original information about pesticide behaviour and impact in periphytic microorganisms.
Diuron-induced rat urinary bladder carcinogenesis: mode of action and human relevance evaluations using the International Programme on Chemical Safety framework
Crit Rev Toxicol 2014 May;44(5):393-406.PMID:24512549DOI:10.3109/10408444.2013.877870.
Diuron, a high volume substituted urea herbicide, induced high incidences of urinary bladder carcinomas and low incidences of kidney pelvis papillomas and carcinomas in rats exposed to high doses (2500 ppm) in a 2-year bioassay. Diuron is registered for both occupational and residential uses and is used worldwide for more than 30 different crops. The proposed rat urothelial mode of action (MOA) for this herbicide consists of metabolic activation to metabolites that are excreted and concentrated in the urine, leading to cytotoxicity, urothelial cell necrosis and exfoliation, regenerative hyperplasia, and eventually tumors. We show evidence for this MOA for Diuron using the International Programme on Chemical Safety (IPCS) conceptual framework for evaluating an MOA for chemical carcinogens, and the United States Environmental Protection Agency (USEPA) and IPCS framework for assessing human relevance.
Toxic Effects Induced by Diuron and Its Metabolites in Caenorhabditis elegans
Neurotox Res 2022 Dec;40(6):1812-1823.PMID:36306114DOI:10.1007/s12640-022-00596-2.
The toxicity of Diuron herbicide and its metabolites has been extensively investigated; however, their precise toxic mechanisms have yet to be fully appreciated. In this context, we evaluated the toxic mechanism of Diuron, 3,4-dichloroaniline (DCA) and 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU), using Caenorhabditis elegans (C. elegans) in the L1 larval stage. For this purpose, worms were acutely exposed to the test chemicals with a preliminary concentration range of 0.5 to 500 μM and first analyzed for lethality (%). Next, the highest concentration (500 μM) was considered for survival (%), reactive oxygen and nitrogen species (RONS), glutathione (GSH) and ATP levels, autophagy index, behavior, and dopaminergic neurodegeneration parameters. Interestingly, increased lethality (%) was found for all chemicals at the higher concentrations tested (100 and 500 μM), with significant differences at 500 μM DCA (p < 0.05). A decrease in the median survival was observed mainly for DCA. Although no changes were observed in RONS production, GSH levels were significantly increased upon Diuron and DCA treatment, likely reflecting an attempt to restore the redox status. Moreover, Diuron and its metabolites impaired ATP levels, suggesting an alteration in mitochondrial function. The latter may trigger autophagy as an adaptive survival mechanism, but this was not observed in C. elegans. Dopaminergic neurotoxicity was observed upon treatment with all the tested chemicals, but only Diuron induced alterations in the worms' locomotor behavior. Combined, these results indicate that exposure to high concentrations of Diuron and its metabolites elicit distinct adverse outcomes in C. elegans, and DCA in particular, plays an important role in the overall toxicity observed in this experimental model.