Nivalenol
(Synonyms: 雪腐镰刀菌烯醇) 目录号 : GC44409
A trichothecene mycotoxin
Cas No.:23282-20-4
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nivalenol, classified as type B trichotecenes toxins produced by Fusarium graminearum, is a fungal metabolite present in agricultural product[1]. Nivalenol induces cell death through caspase-dependent mechanisms and via the intrinsic apoptotic pathway. Nivalenol affects the immune system, causes emesis, growth retardation, reproductive disorders and has a haematotoxic/myelotoxic effect[2].
References:
[1]. Bryła M, et al. Natural Occurrence of Nivalenol, Deoxynivalenol, and Deoxynivalenol-3-Glucoside in Polish Winter Wheat. Toxins (Basel). 2018 Feb 13;10(2).
[2]. Aupanun S, et al. Individual and combined mycotoxins deoxynivalenol, nivalenol, and fusarenon-X induced apoptosis in lymphoid tissues of mice after oral exposure. Toxicon. 2019 Jul;165:83-94.
| Cas No. | 23282-20-4 | SDF | |
| 别名 | 雪腐镰刀菌烯醇 | ||
| Canonical SMILES | CC1=C[C@]2([H])[C@]([C@]3(C)[C@@]4(OC4)[C@]([C@H](O)[C@H]3O)([H])O2)(CO)[C@H](O)C1=O | ||
| 分子式 | C15H20O7 | 分子量 | 312.3 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 25 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): 10 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.202 mL | 16.0102 mL | 32.0205 mL |
| 5 mM | 0.6404 mL | 3.202 mL | 6.4041 mL |
| 10 mM | 0.3202 mL | 1.601 mL | 3.202 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。
Nivalenol Mycotoxin Concerns in Foods: An Overview on Occurrence, Impact on Human and Animal Health and Its Detection and Management Strategies
Toxins (Basel) 2022 Jul 31;14(8):527.PMID:36006189DOI:10.3390/toxins14080527.
Mycotoxins are secondary metabolites produced by fungi that infect a wide range of foods worldwide. Nivalenol (NIV), a type B trichothecene produced by numerous Fusarium species, has the ability to infect a variety of foods both in the field and during post-harvest handling and management. NIV is frequently found in cereal and cereal-based goods, and its strong cytotoxicity poses major concerns for both human and animal health. To address these issues, this review briefly overviews the sources, occurrence, chemistry and biosynthesis of NIV. Additionally, a brief overview of several sophisticated detection and management techniques is included, along with the implications of processing and environmental factors on the formation of NIV. This review's main goal is to offer trustworthy and current information on NIV as a mycotoxin concern in foods, with potential mitigation measures to assure food safety and security.
Deoxynivalenol and Nivalenol Toxicities in Cultured Cells: a Review of Comparative Studies
Food Saf (Tokyo) 2018 May 25;6(2):51-57.PMID:32231947DOI:10.14252/foodsafetyfscj.2017026.
The in vitro studies of the toxicities of trichothecene mycotoxins deoxynivalenol (DON) and Nivalenol (NIV) including cell proliferation, cytokine secretion, and the involvement of heat shock protein 90 (Hsp90) in their toxicities were reviewed. Trichothecene mycotoxins are extremely toxic to leukocytes and leukopenia is one of the leading signs of trichothecene toxicosis, implying that trichothecenes hinder cell proliferation. Both toxins retarded proliferation of all four cell lines tested. NIV was more potent than DON in human promyelocytic leukemia cell line HL60, human lymphoblastic leukemia cell line MOLT-4, and rat aortic myoblast cell line A-10. In contrast, both toxins exhibited almost the same potencies in human hepatoblastoma cell line HepG2. While exposure to 0.3 μg/mL DON greatly induced the secretion of anti-hematopoietic cytokines CCL3 and CCL4, treatment with NIV decreased the secretion of these cytokines in HL60 cells, indicating that the toxicity mechanisms of these mycotoxins differ. Because molecular chaperone Hsp90 occupies a pivotal position in a wide range of pathological processes, the effects of an Hsp90-specific inhibitor radicicol on cytokine secretions were investigated. Radicicol counteracted the effect of DON on cytokine secretion, indicating that Hsp90 plays a crucial role in DON-induced cytokine secretion in HL60 cells. Conversely, the results of co-treatment with NIV and radicicol indicate that radicicol does not mitigate the effect of NIV. Regarding CCL3 and CCL4 secretions, DON and NIV have Hsp90-related and -unrelated mechanisms of toxicities, respectively. Taken together the results suggest that, although these toxins share similar chemical structure, there are differences in their toxic mechanisms.
Nivalenol affects spindle formation and organelle functions during mouse oocyte maturation
Toxicol Appl Pharmacol 2022 Feb 1;436:115882.PMID:35016910DOI:10.1016/j.taap.2022.115882.
Oocyte maturation is essential for fertilization and early embryo development, and proper organelle functions guarantee this process to maintain high-quality oocytes. The type B trichothecene Nivalenol (NIV) is a mycotoxin produced by Fusarium oxysporum and is commonly found in contaminated food. NIV intake affect growth, the immune system, and the female reproductive system. Here, we investigated NIV toxicity on mouse oocyte quality. Transcriptome analysis results showed that NIV exposure altered the expression of multiple genes involved in spindle formation and organelle function in mouse oocytes, indicating its toxicity on mouse oocyte maturation. Further analysis indicated that NIV exposure disrupted spindle structure and chromosome alignment, possibly through tubulin acetylation. NIV exposure induced aberrant mitochondria distribution and reduced mitochondria number, mitochondria membrane potential (MMP), and ATP levels. In addition, NIV caused the abnormal distribution of the Golgi apparatus and altered the expression of the vesicle trafficking protein Rab11. ER distribution was also disturbed under NIV exposure, indicating the effects of NIV on protein modification and transport in oocytes. Thus, our results demonstrated that NIV exposure affected spindle structure and organelles function in mouse oocytes.
Occurrence, mitigation and in vitro cytotoxicity of Nivalenol, a type B trichothecene mycotoxin - Updates from the last decade (2010-2020)
Food Chem Toxicol 2021 Jun;152:112182.PMID:33838177DOI:10.1016/j.fct.2021.112182.
The present review aims to give an overview of the literature of the last decade (2010-2020) concerning the occurrence of the type B trichothecene mycotoxin Nivalenol (NIV) and its in vitro toxicity, with the purpose of updating information regarding last researches on this mycotoxin. The most recent studies on the possible methods for preventing Fusarium spp. growth and NIV production are also discussed. Recently, various environmental factors have been shown to influence strongly NIV occurrence. However, Fusarium spp. of the NIV genotype have been found almost worldwide. With regard to NIV cytotoxicity, NIV has been reported to cause a marked decrease in cell proliferation in different mammalian cells. In particular, the recent data suggest that organs containing actively proliferating cells represent the main targets of NIV. Moreover, NIV resulted to cause immunosuppression, gastrointestinal toxicity and genotoxicity. However, sufficient evidence of carcinogenicity in humans is currently lacking, and the International Agency for Research on Cancer (IARC) classifies it as a group 3 carcinogen. Further researches and the discovery of effective treatment strategies to prevent NIV contamination and to counteract its toxicity are urgently required against this common food-borne threat to human health and livestock.
Metabolism of Nivalenol and nivalenol-3-glucoside in rats
Toxicol Lett 2019 May 15;306:43-52.PMID:30769082DOI:10.1016/j.toxlet.2019.02.006.
Plant-derived mycotoxin conjugates like deoxynivalenol-3-glucoside can be partly hydrolyzed to their aglycones in vivo, albeit to different extent depending on the mycotoxin conjugate and on the animal species. The aim of this work was to investigate the metabolization of the trichothecene mycotoxin Nivalenol (NIV) and the fate of its modified form NIV-3-glucoside (NIV3G) in rats. To that end, 350 μg/kg body weight of NIV and the equimolar dose of NIV3G were administered to six rats by gavage in a 5 × 6 design and excreta were collected for 2 days after each treatment. For further analysis of NIV and NIV3G metabolites in rat urine and feces, seven novel NIV- and NIV3G metabolites including NIV sulfonates (NIVS) 1, 2 and 3, deepoxy-NIV (DNIV), DNIV sulfonate 2, NIV3G sulfonate (NIV3GS) 2 and NIV-3-glucuronide were produced, isolated and characterized. Subsequently, LC-MS/MS based methods for determination of NIV, NIV3G and their metabolites in excreta samples were developed, validated and applied. The biological recoveries of administered toxins in the form of their fecal and urinary metabolites were 57 ± 21% for NIV and 94 ± 36% for NIV3G. The majority of NIV and NIV3G metabolites was excreted into feces, with DNIV and NIVS 2 as major NIV metabolites and NIV3GS 2 and DNIV as major metabolites of NIV3G. Only 1.5% of the administered NIV3G was recovered in urine, with NIV3G itself as major urinary metabolite. The biological recovery of free NIV in urine was approximately 30 times lower after treatment with NIV3G than after administration of NIV, indicating that exposure of rats to NIV3G results in lower toxicity than exposure to NIV.