Agaric acid
(Synonyms: 落叶松蕈酸,Agaricinic Acid) 目录号 : GC63642
Agaric acid (Agaricinic Acid) 来自真菌部落的 Polyporus officinalis 和 Polyporus igniarius。Agaric acid 通过其与腺嘌呤核苷酸转位酶的相互作用诱导线粒体通透性转变。Agaric acid 可促进积累的 Ca2+ 流出，跨膜电位的破坏和线粒体肿胀。Agaric acid 用于调节脂类代谢。
Cas No.:666-99-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Agaric acid (Agaricinic Acid) is obtained from various plants of the fungous tribe, i.e. Polyporus officinalis and Polyporus igniarius. Agaric acid induces mitochondrial permeability transition through its interaction with the adenine nucleotide translocase. Agaric acid promotes efflux of accumulated Ca2+, collapse of transmembrane potential, and mitochondrial swelling. Agaric acid is used to regulate lipid metabolism[1].
[1]. GarcÍa N, et al. Agaric acid induces mitochondrial permeability transition through its interaction with the adenine nucleotide translocase. Its dependence on membrane fluidity. Mitochondrion. 2005 Aug;5(4):272-81.
| Cas No. | 666-99-9 | SDF | |
| 别名 | 落叶松蕈酸,Agaricinic Acid | ||
| 分子式 | C22H40O7 | 分子量 | 416.55 |
| 溶解度 | DMSO : 125 mg/mL (300.08 mM; Need ultrasonic) | 储存条件 | 4°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。 |
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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 | 2.4007 mL | 12.0034 mL | 24.0067 mL |
| 5 mM | 0.4801 mL | 2.4007 mL | 4.8013 mL |
| 10 mM | 0.2401 mL | 1.2003 mL | 2.4007 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。
Agaric acid reduces Salmonella biofilm formation by inhibiting flagellar motility
Biofilm 2020 May 29;2:100022.PMID:33447808DOI:10.1016/j.bioflm.2020.100022.
Salmonella biofilms are a common cause of contaminations in the food or feed industry. In a screening for novel compounds to combat biofilm-associated foodborne outbreaks, we identified Agaric acid as a Salmonella Typhimurium biofilm inhibitor that does not affect planktonic growth. Importantly, the remaining biofilm cells after preventive treatment with Agaric acid were significantly more sensitive to the common disinfectant hydrogen peroxide. Screening of a GFP-promoter fusion library of biofilm related genes revealed that Agaric acid downregulates the transcription of genes responsible for flagellar motility. Concurrently, swimming motility was completely abrogated in the presence of Agaric acid, indicating that biofilm inhibition occurs via interference with the motility phenotype. Moreover, Agaric acid also reduced biofilm formation of Pseudomonas aeruginosa, Staphylococcus aureus and Escherichia coli. Agaric acid thus shows potential as an anti-virulence compound that inhibits both motility and biofilm formation.
Interaction of Agaric acid with the Adenine Nucleotide Translocase Induces Mitochondrial Oxidative Stress
Biochem Res Int 2020 Dec 22;2020:5253108.PMID:33489376DOI:10.1155/2020/5253108.
Mitochondrial permeability transition is characterized by the opening of a transmembranal pore that switches membrane permeability from specific to nonspecific. This structure allows the free traffic of ions, metabolites, and water across the mitochondrial inner membrane. The opening of the permeability transition pore is triggered by oxidative stress along with calcium overload. In this work, we explored if oxidative stress is a consequence, rather than an effector of the pore opening, by evaluating the interaction of Agaric acid with the adenine nucleotide translocase, a structural component of the permeability transition pore. We found that Agaric acid induces transition pore opening, increases the generation of oxygen-derived reactive species, augments the oxidation of unsaturated fatty acids in the membrane, and promotes the detachment of cytochrome c from the inner membrane. The effect of Agaric acid was inhibited by the antioxidant tamoxifen in association with decreased binding of the thiol reagent eosin-3 maleimide to the adenine nucleotide translocase. We conclude that Agaric acid promotes the opening of the pore, increasing ROS production that exerts oxidative modification of critical thiols in the adenine nucleotide translocase.
Agaric acid induces mitochondrial permeability transition through its interaction with the adenine nucleotide translocase. Its dependence on membrane fluidity
Mitochondrion 2005 Aug;5(4):272-81.PMID:16050990DOI:10.1016/j.mito.2005.05.002.
The effect of Agaric acid as inducer of mitochondrial permeability transition was studied. It was found that: (i) Agaric acid (AA) promoted efflux of accumulated Ca2+, collapse of transmembrane potential, and mitochondrial swelling; (ii) these effects depend on membrane fluidity; (iii) ADP inhibited the effect of AA on Ca2+ efflux, and (iv) AA blocked binding of the sulfhydryl reagent, eosin-5-maleimide, to the adenine nucleotide translocase. It is proposed that AA induces pore opening through binding of the citrate moiety to the ADP/ATP carrier; this interaction must be stabilized by insertion of the alkyl chain in the lipid milieu of the membrane.
The effect of N-ethylmaleimide on permeability transition as induced by carboxyatractyloside, Agaric acid, and oleate
Cell Biochem Biophys 2008;51(2-3):81-7.PMID:18649145DOI:10.1007/s12013-008-9016-5.
In this work, we studied the effect of N-ethylmaleimide on permeability transition. The findings indicate that the amine inhibited the effects of carboxyatractyloside and Agaric acid. It is known that these reagents interact with the adenine nucleotide carrier through the cytosolic side. When oleate, which interacts through the matrix side, was used it was found that the amine amplified the effects of oleate on permeability transition. The results also show that N-ethylmaleimide strengthened the inhibition induced by carboxyatractyloside, Agaric acid, and oleate on ADP exchange. Furthermore, it was also found that oleate improved the binding of eosin-5-maleimide on the adenine nucleotide translocase.
Aurintricarboxylic acid is a potent inhibitor of phosphofructokinase
Biochem J 1989 May 1;259(3):925-7.PMID:2525029DOI:10.1042/bj2590925.
Aurintricarboxylic acid (ATA) was found to be a very potent inhibitor of purified rabbit liver phosphofructokinase (PFK), giving 50% inhibition at 0.2 microM. The inhibition was in a manner consistent with interaction at the citrate-inhibitory site of the enzyme. The data suggest that inhibition of PFK by ATA was not due to denaturation of the enzyme or the irreversible binding of inhibitor, since the inhibition could be reversed by addition of allosteric activators of PFK, i.e. fructose 2,6-bisphosphate or AMP. Two other tricarboxylic acids, Agaric acid and (-)-hydroxycitrate, were found to inhibit PFK. ATA at much higher concentrations (500 microM) was shown to inhibit fatty acid synthesis from endogenous glycogen in rat hepatocytes; however, protein synthesis was not altered.