Fusaric Acid
(Synonyms: 萎蔫酸) 目录号 : GC18061
A mycotoxin
Cas No.:536-69-6
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
| Cell experiment [1]: | |
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Cell lines |
Tobacco suspension cells |
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Preparation Method |
Tobacco suspension cells were treated with 100 μM fusaric acid and then analyzed for H2O2 accumulation and mitochondrial functions. |
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Reaction Conditions |
100 μM; 240 min |
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Applications |
Cells undergoing fusaric acid-induced programmed cell death exhibited H2O2 production, lipid peroxidation, and a decrease of the catalase and ascorbate peroxidase activities. |
| Animal experiment [2]: | |
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Animal models |
crossbred barrows |
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Preparation Method |
A total of 40 crossbred barrows (initial weight 10 kg) were orally dosed with 0 or 200 mg of fusaric acid/kg of BW and five animals from each treatment were killed 4.5, 9, 18, or 36 h after dosing. Animals in the group killed 36 h after dosing were observed for behavioral changes. |
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Dosage form |
0 or 200 mg/kg; orally |
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Applications |
Vomiting was noted in 60% of the pigs dosed with fusaric acid.The major neurochemical changes due to exposure to fusaric acid were seen in the hypothalamus 18 h after dosing.Brain tryptophan, serotonin, and 5-hydroxyindoleacetic acid all tended to be elevated by the action of fusaric acid. |
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References: [1]. Jiao J, et al. Hydrogen peroxide production and mitochondrial dysfunction contribute to the fusaric acid-induced programmed cell death in tobacco cells. J Plant Physiol. 2014 Aug 15;171(13):1197-203. [2]. Smith TK, et al. Effect of fusaric acid on brain regional neurochemistry and vomiting behavior in swine. J Anim Sci. 1991 May;69(5):2044-9. |
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Fusaric acid, as a mycotoxin produced by the Fusarium species, has diverse toxicological effects in plants and animals.[1]
In vitro, treatment with 104 μg/ml fusaric acid in human hepatocellular carcinoma (HepG2) cells post-translationally activates p53 in response to DNA damage.[2] In vitro efficacy test it shown that in HepG2 cells fusaric acid remarkably increased p53 promoter methylation in the 25, 104, and 150 μg/ml fusaric acid treatments; but in the 50 μg/ml fusaric acid treatment significantly decreased the promoter methylation of p53. [1] In HepG2 cells, fusaric acid dramatically increased promoter methylation of DNMT1 compared to the control; however, treatment with 25, 50, and 104 μg/ml fusaric acid decreased the promoter methylation of DNMT3A and treatment with 150 μg/ml increased the promoter methylation of DNMT3A.[3] Fusaric acid has toxicity (24 h incubation; IC50 = 104 μg/ml) on mitochondrial output, cellular and mitochondrial stress responses, mitochondrial biogenesis and markers of cell death.[4] In addition, fusaric acid has cytotoxicity to PBMCs with IC50 of 240.8?μg/ml and Thp-1 with IC50 of 107.7?μg/ml cells at 24?h.[5]
In vivo experiment it indicated that treatment with 100 mg/kg body weight fusaric acid intraperitoneally 30 min prior to the onset of the dark phase (lights out) in rats increased the level of brain serotonin (5HT), 5-hydroxyindoleacetic acid (5HIAA), tyrosine (TYRO), and dopamine (DA) and decreased the level of norepinephrine (NEpi).[6]
References:
[1]Ghazi T, et al. Fusaric acid decreases p53 expression by altering promoter methylation and m6A RNA methylation in human hepatocellular carcinoma (HepG2) cells. Epigenetics. 2021 Jan;16(1):79-91.
[2]Ghazi T, Nagiah S, Tiloke C, et al. Fusaric acid induces DNA damage and post‐translational modifications of p53 in human hepatocellular carcinoma (HepG2) cells. J Cell Biochem. 2017. November;118(11):3866–3874.
[3]Ghazi T, et al. Fusaric acid-induced promoter methylation of DNA methyltransferases triggers DNA hypomethylation in human hepatocellular carcinoma (HepG2) cells. Epigenetics. 2019 Aug;14(8):804-817.?
[4]Sheik Abdul N, et al. Fusaric acid induces mitochondrial stress in human hepatocellular carcinoma (HepG2) cells. Toxicon. 2016 Sep 1;119:336-44.?
[5]Dhani S, et al. Fusaric Acid immunotoxicity and MAPK activation in normal peripheral blood mononuclear cells and Thp-1 cells. Sci Rep. 2017 Jun 8;7(1):3051.
[6]Porter JK, et al. Fusaric acid in Fusarium moniliforme cultures, corn, and feeds toxic to livestock and the neurochemical effects in the brain and pineal gland of rats. Nat Toxins. 1995;3(2):91-100.
镰刀菌酸是一种由镰刀菌产生的真菌毒素，对动植物具有多种毒理作用。[1]
在体外，用 104 μg/ml 镰刀菌酸处理人肝细胞癌 (HepG2) 细胞后翻译后激活 p53 以响应 DNA 损伤。[2] 体外功效测试表明在 HepG2 细胞中，镰刀菌酸在 25、104 和 150 μg/ml 镰刀菌酸处理中显着增加 p53 启动子甲基化；但在 50 μg/ml 镰刀菌酸处理中显着降低了 p53 的启动子甲基化。 [1] 在 HepG2 细胞中，与对照相比，镰刀菌酸显着增加了 DNMT1 的启动子甲基化；然而，用 25、50 和 104 μg/ml 的镰刀菌酸处理降低了 DNMT3A 的启动子甲基化，用 150 μg/ml 的处理增加了 DNMT3A 的启动子甲基化。[3] 镰刀菌酸具有毒性（孵育 24 小时；IC50 = 104 μg/ml) 对线粒体输出、细胞和线粒体应激反应、线粒体生物合成和细胞死亡标志物的影响。[4] 此外，镰刀菌酸对 PBMCs 具有细胞毒性，IC50 为 240.8μg/ml，Thp-1 的 IC50 为 107.7μg/ml 细胞，在 24>h。[5 ]
体内实验表明，在大鼠黑暗阶段（熄灯）开始前 30 分钟腹腔注射 100 mg/kg 镰刀菌酸可增加脑血清素 (5HT)、5-羟基吲哚乙酸的水平(5HIAA)、酪氨酸 (TYRO) 和多巴胺 (DA)，并降低去甲肾上腺素 (NEpi) 的水平。[6]
| Cas No. | 536-69-6 | SDF | |
| 别名 | 萎蔫酸 | ||
| 化学名 | 5-butyl-2-pyridinecarboxylic acid | ||
| Canonical SMILES | O=C(O)C1=CC=C(CCCC)C=N1 | ||
| 分子式 | C10H13NO2 | 分子量 | 179.2 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): 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 | 5.5804 mL | 27.9018 mL | 55.8036 mL |
| 5 mM | 1.1161 mL | 5.5804 mL | 11.1607 mL |
| 10 mM | 0.558 mL | 2.7902 mL | 5.5804 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。
Fusaric acid detoxification: a strategy of Gliocladium roseum involved in its antagonism against Fusarium verticillioides
Fungal co-culture has several biotechnological applications including the discovery or the enhanced production of secondary metabolites. It is also a powerful tool aiding to elucidate the involvement of secondary metabolism in fungus-fungus interactions. The aim of this work was to investigate secondary metabolites produced when Fusarium verticillioides is co-cultured with Gliocladium roseum. Secreted metabolites were analyzed by HPLC-MS, and fusaric acid (FA) was quantified by HPLC-DAD. Four FA derivatives were identified only in the F. verticillioides-G. roseum co-culture. Mass spectrometry and one- and two-dimensional NMR spectra indicated that they were 5-butylpyridine-2-carboxylic acid methyl ester (5B2CAM), 4-(5-butylpicolinamido) butanoic acid (45BBA), methyl 4-(5-butylpicolinamido) butanoate (M45BBA), and bis(5-butyl-2-pyridinecarboxylate-N1,O2)-copper (B52P). 45BBA and M45BBA are reported for the first time and were FA biotransformation products generated by G. roseum. The antifungal activity of 5B2CAM, 45BBA, and M45BBA was evaluated in vitro against Botrytis cinerea and Aspergillus niger. They were less fungitoxic than FA, with 45BBA as the least toxic. Our results suggest that the effective antagonism exerted by G. roseum against F. verticillioides is due, at least in part, to its detoxifying ability against FA.
Fusaric acid induces hepatic global m6A RNA methylation and differential expression of m6A regulatory genes in vivo - a pilot study
N6-methyladenosine (m6A) is an abundant epitranscriptomic mark that regulates gene expression to execute cellular developmental programmes and environmental adaptation. Fusaric acid (FA) is a mycotoxin that contaminates agricultural foods and exerts toxicity in humans and animals; however, its epitranscriptomic effects are unclear. We investigated the effect of FA on global m6A RNA methylation and mRNA expression levels of key m6A regulatory genes in C57BL/6 mouse livers. C57BL/6 mice (n = 6/group) were orally administered 0.1 M phosphate-buffered saline (PBS) or 50 mg/kg FA. Mice were euthanized 24 h after oral administration, livers were harvested, and RNA was isolated. RNA samples were assayed for global m6A levels using an m6A RNA Methylation Quantification Kit. The mRNA expression of m6A regulators i.e. writers, erasers, and readers were measured by qRT-PCR. FA increased global m6A RNA methylation (p < 0.0001) in mouse livers. FA increased the expression of METTL3 (p = 0.0143) and METTL14 (p = 0.0281), and decreased the expression of FTO (p = 0.0036) and ALKBH5 (p = 0.0035). The expression of YTHDF2 (p = 0.0007), YTHDF3 (p = 0.0061), and YTHDC2 (p = 0.0258) were increased by FA in mouse livers. This study shows that the liver m6A epitranscriptome can be modified by FA exposure in an in vivo model and can be useful for identifying the molecular mechanisms whereby m6A RNA modifications influence the toxicological outcomes of FA exposure.
The Fusaric Acid Derivative qy17 Inhibits Staphylococcus haemolyticus by Disrupting Biofilm Formation and the Stress Response via Altered Gene Expression
Staphylococcus haemolyticus (S. haemolyticus) is the second most commonly isolated coagulase-negative staphylococcus (CoNS) in patients with hospital-acquired infections. It can produce phenol-soluble modulin (PSM) toxins and form biofilms. Compared with the wealth of information on Staphylococcus aureus and Staphylococcus epidermidis, very little is known about S. haemolyticus. There is an urgent need to find an effective preparation to combat the harm caused by S. haemolyticus infection. Chinese herbs have been utilized to cure inflammation and infectious diseases and have a long history of anticancer function in China. Here, we modified fusaric acid characterized from the metabolites of Gibberella intermedia, an endophyte previously isolated from Polygonum capitatum. This study shows that fusaric acid analogs (qy17 and qy20) have strong antibacterial activity against S. haemolyticus. In addition, crystal violet analyses and scanning electron microscopy observations demonstrated that qy17 inhibited biofilm formation and disrupted mature biofilms of S. haemolyticus in a dose-dependent manner. Additionally, it reduced the number of live bacteria inside the biofilm. Furthermore, the antibiofilm function of qy17 was achieved by downregulating transcription factors (sigB), transpeptidase genes (srtA), and bacterial surface proteins (ebp, fbp) and upregulating biofilm-related genes and the density-sensing system (agrB). To further elucidate the bacteriostatic mechanism, transcriptomic analysis was carried out. The following antibacterial mechanisms were uncovered: (i) the inhibition of heat shock (clpB, groES, groL, grpE, dnaK, dnaJ)-, oxidative stress (aphC)- and biotin response (bioB)-related gene expression, which resulted in S. haemolyticus being unable to compensate for various stress conditions, thereby affecting bacterial growth; and (ii) a reduction in the expression of PSM-beta (PSMβ1, PSMβ2, PSMβ3) toxin- and Clp protease (clpP, clpX)-related genes. These findings could have major implications for the treatment of diseases caused by S. haemolyticus infections. Our research reveals for the first time that fusaric acid derivatives inhibit the expression of biofilm formation-related effector and virulence genes of S. haemolyticus. These findings provide new potential drug candidates for hospital-acquired infections caused by S. haemolyticus.
Pharmacological activities of fusaric acid (5-butylpicolinic acid)
This review article aims at summarizing research findings on the various pharmacological activities of fusaric acid (5-butylpicolinic acid), a mycotoxin produced by several Fusarium species which commonly infect cereal grains and other agricultural commodities. The actions of the toxin on mammals, birds, arthropods, crustaceans and plants are covered. The effects on mammals are diverse and are apparent in the nervous, cardiovascular and immune systems. Fusaric acid is toxic to some mammalian tumor cell lines.
Fusaric acid decreases p53 expression by altering promoter methylation and m6A RNA methylation in human hepatocellular carcinoma (HepG2) cells
Fusaric acid (FA) is a food-borne mycotoxin that mediates toxicity with limited information on its epigenetic properties. p53 is a tumour suppressor protein that regulates cell cycle arrest and apoptotic cell death. The expression of p53 is regulated transcriptionally by promoter methylation and post-transcriptionally by N-6-methyladenosine (m6A) RNA methylation. We investigated the effect of FA on p53 expression and its epigenetic regulation via promoter methylation and m6A RNA methylation in human hepatocellular carcinoma (HepG2) cells. HepG2 cells were treated with FA [0, 25, 50, 104, and 150 ?g/ml; 24 h] and thereafter, DNA, RNA, and protein was isolated. Promoter methylation and expression of p53 was measured using qPCR and Western blot. RNA immuno-precipitation was used to determine m6A-p53 levels. The expression of m6A methyltransferases (METTL3 and METTL14), demethylases (FTO and ALKBH5), and readers (YTHDF1-3 and YTHDC2) were measured using qPCR. FA induced p53 promoter hypermethylation (p < 0.0001) and decreased p53 expression (p < 0.0001). FA decreased m6A-p53 levels (p < 0.0001) by decreasing METTL3 (p < 0.0001) and METTL14 (p < 0.0001); and suppressed expression of YTHDF1 (p < 0.0001), YTHDF3 (p < 0.0001), and YTHDC2 (p < 0.0001) that ultimately reduced p53 translation (p < 0.0001). Taken together, the data shows that FA epigenetically decreased p53 expression by altering its promoter methylation and m6A RNA methylation in HepG2 cells. This study reveals a mechanism for p53 regulation by FA and provides insight into future therapeutic interventions.