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<compound>
  <id type="integer">3791</id>
  <title>T3D3737</title>
  <common-name>Citreoviridin A</common-name>
  <description>Citreoviridin A is an exogenous solid with the formula C23H30O6 and an average molecular weight of 402.48 g/mol. Citreoviridin A belongs to the pyranones and derivatives, a subclass of pyrans within the organic compounds. It functions biologically as a mycotoxin (PMC7077241). Health effects associated with this compound include cardiomyopathy (PMC7077241), paralysis (PMC7077241), respiratory failure (PMC7077241), and Keshan disease (PMC7077241).

The compound interacts with 15 recorded protein targets. These include the Sodium/potassium-transporting ATPase subunits gamma (FXYD2), alpha-1 (ATP1A1), alpha-2 (ATP1A2), and alpha-3 (ATP1A3); citreoviridin inhibits synaptosomal Na+/K+-ATPase, which alters synaptic transmission. It also binds to the beta subunit of the mitochondrial ATP synthase F(1) complex (ATP5F1B), inhibiting mitochondrial energy-linked reactions such as ATP-driven reduction of NAD+ by succinate, ATP-driven NAD transhydrogenase, and ADP-stimulated respiration. Additionally, citreoviridin interacts with Solute carrier family 22 members 1 (SLC22A1), 2 (SLC22A2), 6 (SLC22A6), and 11 (SLC22A11), as well as two other proteins. Mycotoxins may enter the kidney and liver via human organic cation transporters (hOCTs) and human organic anion transporters (hOATs), where they can inhibit the uptake of cations and anions. This interference with the secretion of xenobiotics, drugs, and endogenous metabolites can lead to increased cellular accumulation of toxic compounds, causing hepatotoxicity and nephrotoxicity.</description>
  <cas>25425-12-1</cas>
  <pubchem-id>6436023</pubchem-id>
  <chemical-formula>C23H30O6</chemical-formula>
  <weight nil="true"/>
  <appearance>White powder.</appearance>
  <melting-point>107 - 111°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility nil="true"/>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral, dermal, inhalation, and parenteral (contaminated drugs). (A3101)</route-of-exposure>
  <target nil="true"/>
  <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. (A3002, A3003, A3005, A3006, A3014)</mechanism-of-toxicity>
  <metabolism nil="true"/>
  <toxicity>LD50: 3.6 mg/kg (Subcutaneous, rat) (A3002)
LD50: 7.5 mg/kg (Intraperitoneal, Mouse) (A3002)
LD50: 29 mg/kg (Oral, Mouse) (A3002)</toxicity>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Citreoviridin is a mycotoxin that has been isolated in Peniciilium citreo-viride, P. ochrosalmoneum, and P. pulvullorum. It can be found in contaminated rice grains, as well as corn infested by Eupenicillium
ochrosalmoneurn. (A3002)</use-source>
  <min-risk-level nil="true"/>
  <health-effects>Citreoviridin selectively inhibits motor nerve cells in the medulla oblongata and accumulates in
the grey matter and brain stem. This can cause central nervous system depression leading to respiratory and cardiovascular failures and death. (A3002, A3004, A3005)</health-effects>
  <symptoms>Symptoms of citreoviridin exposure include progressive paralysis, vomiting, convulsions, and gradual
respiratory disorder. (A3002)</symptoms>
  <treatment nil="true"/>
  <created-at type="dateTime">2010-05-06T14:52:05Z</created-at>
  <updated-at type="dateTime">2026-04-03T05:06:40Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia nil="true"/>
  <uniprot-id nil="true"/>
  <kegg-compound-id nil="true"/>
  <omim-id nil="true"/>
  <chebi-id nil="true"/>
  <biocyc-id nil="true"/>
  <ctd-id nil="true"/>
  <stitch-id nil="true"/>
  <drugbank-id nil="true"/>
  <pdb-id nil="true"/>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>[H]/C(=C(/[H])\C(\[H])=C(/[H])C1=C(C)C(OC)=CC(=O)O1)/C(/[H])=C(\[H])/C(/C)=C(\[H])C1(C)OC(C)C(C)(O)C1O</moldb-smiles>
  <moldb-formula>C23H30O6</moldb-formula>
  <moldb-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+</moldb-inchi>
  <moldb-inchikey>JLSVDPQAIKFBTO-USJRQALFSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">402.4807</moldb-average-mass>
  <moldb-mono-mass type="decimal">402.204238692</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp nil="true"/>
  <hmdb-id>HMDB30868</hmdb-id>
  <chembl-id nil="true"/>
  <chemspider-id>4525192</chemspider-id>
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  <structure-image-content-type nil="true"/>
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  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference nil="true"/>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM002706</chemdb-id>
  <dsstox-id nil="true"/>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00018334</susdat-id>
  <iupac nil="true"/>
  <moldb-polar-surface-area>85.22000000000001</moldb-polar-surface-area>
  <moldb-refractivity>118.01279999999998</moldb-refractivity>
  <moldb-polarizability>45.46314193988334</moldb-polarizability>
  <moldb-rotatable-bond-count>6</moldb-rotatable-bond-count>
  <moldb-acceptor-count>5</moldb-acceptor-count>
  <moldb-donor-count>2</moldb-donor-count>
  <moldb-pka-strongest-acidic>12.600983692839542</moldb-pka-strongest-acidic>
  <moldb-pka-strongest-basic>-3.662280515270547</moldb-pka-strongest-basic>
  <moldb-physiological-charge>0</moldb-physiological-charge>
  <moldb-number-of-rings>2</moldb-number-of-rings>
  <moldb-alogps-logp>3.89</moldb-alogps-logp>
  <moldb-alogps-logs>-4.63</moldb-alogps-logs>
  <moldb-alogps-solubility>9.36e-03 g/l</moldb-alogps-solubility>
  <kingdom>Organic compounds</kingdom>
  <superklass>Organoheterocyclic compounds</superklass>
  <klass>Pyrans</klass>
  <subklass>Pyranones and derivatives</subklass>
  <paper-count type="integer">105</paper-count>
  <sync-id>CED0012658</sync-id>
  <structure-inchikey>JLSVDPQAIKFBTO-USJRQALFSA-N</structure-inchikey>
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  <structure-indexed-at type="dateTime">2026-09-19T04:00:54Z</structure-indexed-at>
</compound>
