Cyanazine
(Synonyms: 氰草津) 目录号 : GC60733Cyanazine是一种能抑制植物光合作用的除草剂。Cyanazine是一种选择性的系统性除草剂,用于玉米、豌豆、蚕豆等作物,用于控制多种禾本科杂草和阔叶杂草。
Cas No.:21725-46-2
Sample solution is provided at 25 µL, 10mM.
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Cyanazine is an herbicide which can inhibits photosynthesis of plants. Cyanazine is a selective systemic herbicide for crops such as corn, peas, and broad beans, which is used to control a variety of grass weeds and broadleaf weed[1].
Cyanazine is proved non-genotoxic.
[1]. Gao, S., et al. Preparation and characterization of cyanazine-ydroxypropyl-beta-cyclodextrin inclusion complex. RSC Advances, 2019. 9(45), 26109-26115.
Cas No. | 21725-46-2 | SDF | |
别名 | 氰草津 | ||
Canonical SMILES | CC(C)(NC1=NC(Cl)=NC(NCC)=N1)C#N | ||
分子式 | C9H13ClN6 | 分子量 | 240.69 |
溶解度 | DMSO: 100 mg/mL (415.47 mM) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 4.1547 mL | 20.7736 mL | 41.5472 mL |
5 mM | 0.8309 mL | 4.1547 mL | 8.3094 mL |
10 mM | 0.4155 mL | 2.0774 mL | 4.1547 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 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
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DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
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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。
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Cyanazine herbicide monitoring as a hazardous substance by a DNA nanostructure biosensor
J Hazard Mater 2022 Feb 5;423(Pt A):127058.PMID:34488091DOI:10.1016/j.jhazmat.2021.127058.
Cyanazine is a beneficial herbicide in the triazines group that inhibits photosynthesis in plants and monitoring of this herbicide is so important for study agriculture products. The present researches have been focused on monitoring of Cyanazine by a straightforward and fast electrochemical strategy. Herein, to monitor the Cyanazine level, Pt and Pd doped CdO nanoparticle decorated SWCNTs composite (Pt-Pd-CdO/SWCNTs) has been synthesized as a conductive mediator and characterized by EDS, SEM and TEM techniques. The Pt-Pd-CdO/SWCNTs and ds-DNA have been used for modification of the gold electrode (GE). Moreover, the oxidation signal of guanine relative to ds-DNA at the surface of Pt-Pd-CdO/SWCNTs/ds-DNA/GE has been considered as an bioelectroanalytical issue to monitoring Cyanazine for the first time. Electrochemical impedance spectroscopic (EIS) signals have confirmed that the inclusion of Pt-Pd-CdO/SWCNTs at the surface of the GE has lowered charge-transfer resistance by ca.1.54 times and created a highly conductive state for monitoring of Cyanazine in nanomolar concentration. On the other hand, differential pulse voltammograms (DPV) of Pt-Pd-CdO/SWCNTs/ds-DNA/GE have indicated a linear dynamic range of 4.0 nM-70 µM with a detection limit of 0.8 nM to the monitoring of Cyanazine. In addition, the molecular docking study has emphasized that Cyanazine herbicide is capable of binding to ds-DNA preferably at the guanine-cytosine rich sequences, and confirmed experimental results. In the final step, Pt-Pd-CdO/SWCNTs/ds-DNA/GE has been successfully utilized for the monitoring of Cyanazine herbicide in food and water samples.
Preparation and characterization of cyanazine-hydroxypropyl-beta-cyclodextrin inclusion complex
RSC Adv 2019 Aug 21;9(45):26109-26115.PMID:35531000DOI:10.1039/c9ra04448e.
Due to its poor water solubility, the herbicide Cyanazine is usually dissolved in organic reagents when used, which poses a great threat to the environment. Poor water solubility also causes limited herbicidal activity. In our study, the water solubility of Cyanazine was increased by forming a Cyanazine/hydroxypropyl beta-cyclodextrin (HPβCD) inclusion complex. The formation of the inclusion complex was confirmed by FT-IR, XRD, SEM and other characterization methods. Phase solubility study showed that HPβCD could improve the water solubility of Cyanazine. Thermogravimetric analysis indicated that the thermal stability of Cyanazine was improved by forming inclusion complex and the biological activity test showed that better herbicidal activity was obtained on the inclusion complex compared with the Cyanazine. The results showed that the formation of inclusion complex could improve the application of Cyanazine in agricultural production and reduce the risk to the environment.
Effects of atrazine and Cyanazine on chlorpyrifos toxicity in Chironomus tentans (Diptera: Chironomidae)
Environ Toxicol Chem 2002 Mar;21(3):598-603.PMID:11878473DOI:10.1897/1551-5028(2002)021<0598:eoaaco>2.0.co;2.
Toxicities of two triazine herbicides (atrazine and Cyanazine) and an organophosphate insecticide (chlorpyrifos) were evaluated individually and with each herbicide in binary combination with chlorpyrifos using fourth-instar larvae of the aquatic midge, Chironomus tentans. Chlorpyrifos at 0.25 microg/L resulted in an effect in less than 10% of midges in 48-h acute toxicity bioassays. Neither atrazine nor Cyanazine alone at relatively high concentrations (up to 1,000 microg/L) caused significant acute toxicity to C. tentans. However, atrazine and Cyanazine caused significant synergistic effects on the toxicity of chlorpyrifos when midges were exposed to mixtures of atrazine or Cyanazine (10, 100, 1,000 microg/L) with chlorpyrifos (0.25 microg/L). At fixed concentrations (200 microg/L) of the herbicides, toxicity of chlorpyrifos was enhanced by 1.8- and 2.2-fold by atrazine and Cyanazine, respectively, at the 50% effective concentration levels. Although atrazine and Cyanazine are not effective inhibitors of acetylcholinesterase (AChE) in vitro, the synergism of the two triazine herbicides with chlorpyrifos was associated with increased in vivo inhibition of AChE in midges. We observed a positive correlation between the degree of inhibition of AChE and the concentration of atrazine or Cyanazine in the presence of a fixed concentration of chlorpyrifos. It is possible that these herbicides may affect cytochrome P450 enzymes to confer synergistic effects on the toxicity of chlorpyrifos.
Effects of the chlorotriazine herbicide, Cyanazine, on GABA(A) receptors in cortical tissue from rat brain
Toxicology 1999 Dec 20;142(1):57-68.PMID:10647918DOI:10.1016/s0300-483x(99)00133-x.
Chlorotriazine herbicides disrupt luteinizing hormone (LH) release in female rats following in vivo exposure. Although the mechanism of action is unknown, significant evidence suggests that inhibition of LH release by chlorotriazines may be mediated by effects in the central nervous system. GABA(A) receptors are important for neuronal regulation of gonadotropin releasing hormone and LH release. The ability of chlorotriazine herbicides to interact with GABA(A) receptors was examined by measuring their effects on [3H]muscimol, [3H]Ro15-4513 and [35S]tert-butylbicyclophosphorothionate (TBPS) binding to rat cortical membranes. Cyanazine (1-400 microM) inhibited [3H]Ro15-4513 binding with an IC50 of approximately 105 microM (n=4). Atrazine (1-400 microM) also inhibited [3H]Ro15-4513 binding, but was less potent than Cyanazine (IC50 = 305 microM). However, the chlorotriazine metabolites diaminochlorotriazine, 2-amino-4-chloro-6-ethylamino-s-triazine and 2-amino-4-chloro-6-isopropylamino-s-triazine were without significant effect on [3H]Ro15-4513 binding. Cyanazine and the other chlorotriazines were without effect on [3H]muscimol or [35S]TBPS binding. To examine whether Cyanazine altered GABA(A) receptor function, GABA-stimulated 36Cl- flux into synaptoneurosomes was examined. Cyanazine (50-100 microM) alone did not significantly decrease GABA-stimulated 36Cl- flux. Diazepam (10 microM) and pentobarbital (100 microM) potentiated GABA-stimulated 36Cl- flux to 126 and 166% of control, respectively. At concentrations of 50 and 100 microM, Cyanazine decreased potentiation by diazepam to 112 and 97% of control, respectively, and decreased potentiation by pentobarbital to 158 and 137% of control (n = 6). Interestingly, at lower concentrations (5 microM), Cyanazine shifted the EC50 for GABA-stimulated 36Cl- flux into synaptoneurosomes from 28.9 to 19.4 microM, respectively (n = 5). These results suggest that Cyanazine modulates benzodiazepine, but not the muscimol (GABA receptor site) or TBPS (Cl- channel), binding sites on GABA(A) receptors. Furthermore, at low concentrations, Cyanazine may slightly enhance function of GABA(A) receptors, but at higher concentrations, Cyanazine antagonizes GABA(A) receptor function and in particular antagonizes the positive modulatory effects of diazepam and pentobarbital.
Cancer incidence among pesticide applicators exposed to Cyanazine in the agricultural health study
Environ Health Perspect 2006 Aug;114(8):1248-52.PMID:16882534DOI:10.1289/ehp.8997.
Background: Cyanazine is a common pesticide used frequently in the United States during the 1980s and 1990s. Animal and human studies have suggested that triazines may be carcinogenic, but results have been mixed. We evaluated cancer incidence in cyanazine-exposed pesticide applicators among the 57,311 licensed pesticide applicators in the Agricultural Health Study (AHS). Methods: We obtained detailed pesticide exposure information from a self-administered questionnaire completed at enrollment (1993-1997). Cancer incidence was followed through January 2002. Over half of cyanazine-exposed applicators had >or=6 years of exposure at enrollment, and approximately 85% had begun using Cyanazine before the 1990s. We used adjusted Poisson regression to calculate rate ratios (RRs) and 95% confidence intervals (CIs) of multiple cancer sites among cyanazine-exposed applicators. We calculated ptrend values, and all statistical tests were two-sided. Two exposure metrics were used: tertiles of lifetime days of exposure (LD) and intensity-weighted LD. Results: A total of 20,824 cancer-free AHS applicators reported ever using Cyanazine at enrollment. Cancer incidence comparisons between applicators with the lowest Cyanazine exposure and those with the highest exposure yielded the following for the LD metric: all cancers, RR=0.99 (95% CI, 0.80-1.24); prostate cancer, RR=1.23 (95% CI, 0.87-1.70); all lymphohematopoietic cancers, RR=0.92 (95% CI, 0.50-1.72); non-Hodgkin lymphoma, RR=1.25 (95% CI, 0.47-3.35); lung cancer, RR=0.52 (95% CI, 0.22-1.25). Conclusions: We did not find any clear, consistent associations between Cyanazine exposure and any cancer analyzed. The number of sites was small for certain cancers, limiting any conclusion with regard to ovarian, breast, and some other cancers.