Citreoviridin
(Synonyms: 黄绿青霉素) 目录号 : GC41514A mycotoxin that inhibits the mitochondrial ATPase
Cas No.:25425-12-1
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
Citreoviridin, a toxin from Penicillium citreoviride NRRL 2579, inhibits brain synaptosomal Na+/K+-ATPase whereas in microsomes, both Na+/K+-ATPase and Mg2+-ATPase activities are significantly stimulated in a dose-dependent manner[1]. Citreoviridin inhibits cell proliferation and enhances apoptosis of human umbilical vein endothelial cells[2].
References:
[1]. Datta SC, et al. Effect of citreoviridin, a mycotoxin from Penicillium citreoviride, on kinetic constants of acetylcholinesterase and ATPase in synaptosomes and microsomes from rat brain. Toxicon. 1981;19(4):555-62.
[2]. Hou H, et al. Citreoviridin inhibits cell proliferation and enhances apoptosis of human umbilical vein endothelial cells. Environ Toxicol Pharmacol. 2014 Mar;37(2):828-36.
| Cas No. | 25425-12-1 | SDF | |
| 别名 | 黄绿青霉素 | ||
| Canonical SMILES | O=C1C=C(OC)C(C)=C(/C=C/C=C/C=C/C(C)=C/[C@]2(C)[C@H](O)[C@](O)(C)[C@@H](C)O2)O1 | ||
| 分子式 | C23H30O6 | 分子量 | 402.5 |
| 溶解度 | DMSO: 10 mg/ml,Ethanol: 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。 |
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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 | 2.4845 mL | 12.4224 mL | 24.8447 mL |
| 5 mM | 0.4969 mL | 2.4845 mL | 4.9689 mL |
| 10 mM | 0.2484 mL | 1.2422 mL | 2.4845 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。
[Electrophysiological Effect of Citreoviridin on Human InducedPluripotent Stem Cell-derived Cardiomyocytes]
Shokuhin Eiseigaku Zasshi 2022;63(6):210-217.PMID:36575035DOI:10.3358/shokueishi.63.210.
Citreoviridin (CTV) is a mycotoxin produced by various fungi, including Penicillium citreonigrum. One of the toxicities reportedly associated with CTV is neurotoxicity. CTV is also suspected to be associated with acute cardiac beriberi (also known as "Shoshin-kakke") and Keshan disease, which can have adverse effects on the heart, so the in vivo and in vitro toxicity of CTV on the heart or cardiomyocytes in experimental animal models have been reported. However, the toxicity of CTV for the human heart, especially its electrophysiological effect, remains poorly understood. Therefore, to investigate the electrophysiological effect of CTV on the human cardiomyocytes, we conducted a multi-electrode array (MEA) using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). The MEA revealed that 30 μmol/L of CTV stopped the beating of hiPSC-CMs, and the field potential duration and first peak amplitude were shortened at 10 μmol/L. Before the hiPSC-CMs stopped beating, the length of the inter-spike interval varied two- to four-fold. These results demonstrated that CTV induced an electrophysiological disturbance on human cardiomyocytes. This is first paper to elucidate the electrophysiological effect of CTV on human heart directly and may aid in analyzing the risk associated with CTV to ensure food safety.
Citreoviridin levels in Eupenicillium ochrosalmoneum-infested maize kernels at harvest
Appl Environ Microbiol 1988 May;54(5):1096-8.PMID:3389806DOI:10.1128/aem.54.5.1096-1098.1988.
Citreoviridin contents were measured in eight bulk samples of maize kernels collected from eight fields immediately following harvest in southern Georgia. Citreoviridin contamination in six of the bulk samples ranged from 19 to 2,790 micrograms/kg. In hand-picked samples the toxin was concentrated in a few kernels (pick-outs), the contents of which were stained a bright lemon yellow (range, 53,800 to 759,900 micrograms/kg). The citreoviridin-producing fungus Eupenicillium ochrosalmoneum Scott & Stolk was isolated from each of these pick-out kernels. Citreoviridin was not detected in bulk samples from two of the fields. Aflatoxins were also present in all of the bulk samples (total aflatoxin B1 and B2; range, 7 to 360 micrograms/kg), including those not containing Citreoviridin. In Biotron-grown maize ears that were inoculated with E. ochrosalmoneum through a wound made with a toothpick, Citreoviridin was concentrated primarily in the wounded and fungus-rotted kernels (range, 142,000 to 2,780,000 micrograms/kg). Samples of uninjured kernels immediately adjacent to the wounded kernel (first circle) had less than 4,000 micrograms of Citreoviridin per kg, while the mean concentration of toxin in kernel samples representing the next row removed (second circle) and all remaining kernels from the ear was less than 45 micrograms/kg. Animal toxicosis has not been linked to citreoviridin-contaminated maize.
Citreoviridin, a specific inhibitor of the mitochondiral adenosine triphosphatase
Biochem J 1978 Mar 15;170(3):503-10.PMID:148274DOI:10.1042/bj1700503.
1. Citreoviridin was a potent inhibitor of the soluble mitochondrial ATPase (adenosine triphosphatase) similar to the closely related aurovertins B and D. 2. Citreoviridin inhibited the following mitochondrial energy-linked reactions also: ADP-stimulated respiration in whole mitochondria from ox heart and rat liver; ATP-driven reduction of NAD+ by succinate; ATP-driven NAD transhydrogenase and ATPase from ox heart submitochondrial particles. 3. The dissociation constant (KD) calculated by a simple law-of-mass-action treatment for the citreoviridin--ATPase complex was 0.5--4.2micron for ox-heart mitochondrial preparations and 0.15micron for rat liver mitochondria. 4. Monoacetylation of Citreoviridin decreased its inhibitory potency (KD=2--25micron, ox heart; KD=0.7micron, rat liver). Diacetylation greatly decreased the inhibitory potency (KD=60--215micron, ox heart). 5. Hydrogenation of Citreoviridin monoacetate diminished its inhibitory potency considerably. 6. No significant enhancement of fluorescence was observed when Citreoviridin interacted with the mitochondrial ATPase.
Binding of Citreoviridin to the beta subunit of the yeast F1-ATPase
J Biol Chem 1981 Jan 25;256(2):557-9.PMID:6450205doi
Citreoviridin, a nonfluorescent inhibitor of bovine and bacterial ATPases, also inhibits the yeast F1 (K1 = 2 microM). The beta subunit-specific fluorescent ligand, aurovertin, has been used to report the interaction of Citreoviridin with the yeast F1-ATPase and the isolated beta subunit. Citreoviridin caused a marked decrease in the fluorescence increment associated with the binding of aurovertin to either intact F1 or the isolated beta subunit. Three lines of evidence indicate that Citreoviridin and aurovertin bind to nonidentical sites on the beta subunit: 1) the binding of Citreoviridin to the F1 or isolated beta subunit is noncompetitive with respect to aurovertin; 2) the number of aurovertin binding sites (Kd = 0.2 to 0.6 microM) per F1-ATPase molecule remains the same (1.89 +/- 0.6 mol of aurovertin bound per mol of F1) in the presence or absence of Citreoviridin; 3) the F1-ATPase obtained from the aurovertin-resistant mutant aur-1 is partly inhibited by Citreoviridin.
Citreoviridin induces ROS-dependent autophagic cell death in human liver HepG2 cells
Toxicon 2015 Mar;95:30-7.PMID:25553592DOI:10.1016/j.toxicon.2014.12.014.
Citreoviridin (CIT) is one of toxic mycotoxins derived from fungal species in moldy cereals. Whether CIT exerts hepatotoxicity and the precise molecular mechanisms of CIT hepatotoxicity are not completely elucidated. In this study, the inhibitor of autophagosome formation, 3-methyladenine, protected the cells against CIT cytotoxicity, and the autophagy stimulator rapamycin further decreased the cell viability of CIT-treated HepG2 cells. Knockdown of Atg5 with Atg5 siRNA alleviated CIT-induced cell death. These finding suggested the hypothesis that autophagic cell death contributed to CIT-induced cytotoxicity in HepG2 cells. CIT increased the autophagosome number in HepG2 cells observed under a transmission electron microscope, and this effect was confirmed by the elevated LC3-II levels detected through Western blot. Reduction of P62 protein levels and the result of LC3 turnover assay indicated that the accumulation of autophagosomes in the CIT-treated HepG2 cells was due to increased formation rather than impaired degradation. The pretreatment of HepG2 cells with the ROS inhibitor NAC reduced autophagosome formation and reversed the CIT cytotoxicity, indicating that CIT-induced autophagic cell death was ROS-dependent. In summary, ROS-dependent autophagic cell death of HpeG2 cells described in this study may help to elucidate the underlying mechanism of CIT cytotoxicity.