Citreoviridin
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| Category | Mycotoxins |
| Catalog number | BBF-04540 |
| CAS | 25425-12-1 |
| Molecular Weight | 402.48 |
| Molecular Formula | C23H30O6 |
| Purity | >97% by HPLC |
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Description
The dominant analogue of a family of tetraene mycotoxins with potent neurotoxic effects, produced by several species of aspergillus and penicillium. It inhibits mitochondrial ATPase and is a causative agent of cardiac beriberi.
Specification
| Synonyms | Citreoviridin A; Citreoviridine; Citreoviridine A; [2S-[2α(1E,3E,5E,7E),3β,4α,5α]]-4-Methoxy-5-methyl-6-[7-methyl-8-(tetrahydro-3,4-dihydroxy-2,4,5-trimethyl-2-furanyl)-1,3,5,7-octatetraenyl]-2H-pyran-2-one; 2,5-Anhydro-1,6-dideoxy-2-C-[(1E,3E,5E,7E)-8-(4-methoxy-5-methyl-2-oxo-2H-pyran-6-yl)-2-methyl-1,3,5,7-octatetraenyl]-4-C-methyl-D-Iditol |
| Storage | Store at -20°C |
| IUPAC Name | 6-[(1E,3E,5E,7E)-8-[(2S,3R,4R,5R)-3,4-dihydroxy-2,4,5-trimethyloxolan-2-yl]-7-methylocta-1,3,5,7-tetraenyl]-4-methoxy-5-methylpyran-2-one |
| Canonical SMILES | CC1C(C(C(O1)(C)C=C(C)C=CC=CC=CC2=C(C(=CC(=O)O2)OC)C)O)(C)O |
| InChI | InChI=1S/C23H30O6/c1-15(14-22(4)21(25)23(5,26)17(3)29-22)11-9-7-8-10-12-18-16(2)19(27-6)13-20(24)28-18/h7-14,17,21,25-26H,1-6H3/b8-7+,11-9+,12-10+,15-14+/t17-,21+,22+,23+/m1/s1 |
| InChI Key | JLSVDPQAIKFBTO-OMCRQDLASA-N |
| Source | Citreoviridin is a mycotoxin that has been isolated in Peniciilium citreo-viride, P. ochrosalmoneum, and P. pulvullorum. |
Properties
| Appearance | Yellow to Dark Orange Solid |
| Boiling Point | 585.1±50.0°C at 760 mmHg |
| Melting Point | >100°C (dec.) |
| Density | 1.2±0.1 g/cm3 |
| Solubility | Soluble in Ethanol, Methanol, DMF, DMSO, Chloroform |
Toxicity
| Carcinogenicity | No indication of carcinogenicity to humans (not listed by IARC). |
| Mechanism Of Toxicity | Citreoviridin inhibits both membrane-bound and soluble mitochondrial ATPases. In particular, it inhibits synaptosomal Na+/K+-ATPase, altering synaptic transmission, and binds to the beta subunit of F1-ATPAse. As a result it has been shown to inhibit mitochondrial energy-linked reactions such as ADP-stimulated respiration, ATP-driven reduction of NAD + by succinate, and ATP-driven NAD transhydrogenase. Mycotoxins are often able to enter the liver and kidney by human organic anion transporters (hOATs) and human organic cation transporters (hOCTs). They can also inhibit uptake of anions and cations by these transporters, interfering with the secretion of endogenous metabolites, drugs, and xenobiotics including themselves. This results in increased cellular accumulation of toxic compounds causing nephro- and hepatotoxicity. |
| Toxicity | LD50: 3.6 mg/kg (Subcutaneous, rat); LD50: 7.5 mg/kg (Intraperitoneal, Mouse); LD50: 29 mg/kg (Oral, Mouse). |
Reference Reading
1. Citreoviridin, a specific inhibitor of the mitochondiral adenosine triphosphatase
L J Mulheirn, M D Osselton, A D Mitchell, R B Beechey, P E Linnett Biochem J . 1978 Mar 15;170(3):503-10. doi: 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.
2. Purification and full characterisation of citreoviridin produced by Penicillium citreonigrum in yeast extract sucrose (YES) medium
Mariana Wagner da Rocha, Eloisa Dutra Caldas, Inês Sabioni Resck Food Addit Contam Part A Chem Anal Control Expo Risk Assess . 2015;32(4):584-95. doi: 10.1080/19440049.2014.961177.
The mycotoxin citreoviridin has been associated with the 'yellow rice' disease, which caused cardiac beriberi in Japan. In Brazil, the consumption of contaminated rice was suspected to be involved in a recent beriberi outbreak. In this work, citreoviridin was produced by Penicillium citreonigrum, cultivated in 500 ml yeast extract sucrose (YES) liquid medium for 8 days at 25ºC, and the toxin extracted with chloroform from the liquid medium and the mycelium. A total of 15.3 g of crude extract was obtained from 48 culture flasks, with an estimated citreoviridin contend of 5.54 g, 74.3% being present in the mycelia. Semi-preparative HPLC of the crude extract yielded 27.1% citreoviridin. The HPLC-purified citreoviridin fraction was fully characterised by UV/VIS, FT-IR, (1)H- and (13)C-NMR, LC-MS/MS and LC-MSD TOF, and purity confirmed by gravimetric analysis. Isocitreoviridin was also produced by P. citreonigrum, accounting for about 10% of the citreoviridin present in the crude extract, most transformed into citreoviridin after 10 months under freezing conditions protected from light. Citreoviridin was shown to be stable under the same conditions, although it can suffer isomerisation after a longer storage period. Isomerisation is a potential source of variability in toxicological studies and purity of the material should be checked before study initiation.
3. Binding of citreoviridin to the beta subunit of the yeast F1-ATPase
M G Douglas, E M Gause, M A Buck J Biol Chem . 1981 Jan 25;256(2):557-9.
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.
Spectrum
Predicted LC-MS/MS Spectrum - 10V, Positive
Experimental Conditions
Ionization Mode: Positive
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
