<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">1322</id>
  <title>T3D1318</title>
  <common-name>Ferrous arsenate</common-name>
  <description>Ferrous arsenate is an exogenous inorganic compound with the formula As2Fe3O8 and an average molecular weight of 445.37 g/mol. It exists as a solid at room temperature. Ferrous arsenate belongs to the transition metal arsenates, a subclass of transition metal oxoanionic compounds within the inorganic compounds.

As a mixed metal/non-metal compound, it interacts with numerous protein targets. Arsenic binds to hemoglobin, haptoglobin, the estrogen receptor, and the glucocorticoid receptor. It also binds to actin, including the cytoplasmic 1 and 2 forms as well as the aortic smooth muscle and alpha skeletal muscle forms. Furthermore, arsenic binds to mitochondrial glutathione reductase, which inhibits essential biochemical reactions, alters cellular redox status, and leads to eventual cytotoxicity. Arsenic binding of XPA is believed to induce carcinogenesis by affecting DNA repair.

The compound disrupts ATP production through several mechanisms. Within the citric acid cycle, arsenic inhibits pyruvate dehydrogenase, specifically targeting the mitochondrial dihydrolipoyllysine-residue acetyltransferase component of the pyruvate dehydrogenase complex and the E1 component subunit alpha (both somatic and testis-specific forms) and the E1 component subunit beta. By competing with phosphate, it uncouples oxidative phosphorylation, which inhibits mitochondrial respiration, ATP synthesis, and the energy-linked reduction of NAD+. Additionally, arsenic increases the production of hydrogen peroxide, which may lead to oxidative stress and the formation of reactive oxygen species.</description>
  <cas>10102-50-8</cas>
  <pubchem-id>24938</pubchem-id>
  <chemical-formula>As2Fe3O8</chemical-formula>
  <weight>445.607340</weight>
  <appearance>Green powder.</appearance>
  <melting-point></melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility></solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral (L2) ; inhalation (L2) ; dermal (L2)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (T1, A17)</mechanism-of-toxicity>
  <metabolism>Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (L20)</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>1, carcinogenic to humans. (L135)</carcinogenicity>
  <use-source nil="true"/>
  <min-risk-level>Acute Oral: 0.005 mg/kg/day (L134) 
Chronic Oral: 0.0003 mg/kg/day (L134) 
Chronic Inhalation: 0.01 mg/m3 (L134)</min-risk-level>
  <health-effects>Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (T1, L20)</health-effects>
  <symptoms>Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of </symptoms>
  <treatment>Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (L20)</treatment>
  <created-at type="dateTime">2009-06-19T21:58:36Z</created-at>
  <updated-at type="dateTime">2026-04-05T19:12:34Z</updated-at>
  <interacting-proteins>Metallothionein-2 (P02795) Metallothionein-1G (P13640) Metallothionein-1H (P80294) Metallothionein-3 (P25713) Metallothionein-1F (P04733) Metallothionein-1E (P04732) Metallothionein-1X (P80297) Metallothionein-1A (P04731) Metallothionein-1B (P07438) Metallothionein-1M (Q8N339) Metallothionein-4 (P47944) Metallothionein-1L (Q93083) Arsenite methyltransferase (Q9HBK9) (L92)</interacting-proteins>
  <wikipedia nil="true"/>
  <uniprot-id nil="true"/>
  <kegg-compound-id></kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id></chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>Ferrous arsenate</stitch-id>
  <drugbank-id nil="true"/>
  <pdb-id nil="true"/>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins>
Arsenite methyltransferase (Q9HBK9) 
(L92)</metabolizing-proteins>
  <transporting-proteins>Metallothionein-2 (P02795) 
Metallothionein-1G (P13640) 
Metallothionein-1H (P80294) 
Metallothionein-3 (P25713) 
Metallothionein-1F (P04733) 
Metallothionein-1E (P04732) 
Metallothionein-1X (P80297) 
Metallothionein-1A (P04731) 
Metallothionein-1B (P07438) 
Metallothionein-1M (Q8N339) 
Metallothionein-4 (P47944) 
Metallothionein-1L (Q93083) 
(L92)</transporting-proteins>
  <moldb-smiles>[Fe++].[Fe++].[Fe++].[O-][As]([O-])([O-])=O.[O-][As]([O-])([O-])=O</moldb-smiles>
  <moldb-formula>As2Fe3O8</moldb-formula>
  <moldb-inchi>InChI=1S/2AsH3O4.3Fe/c2*2-1(3,4)5;;;/h2*(H3,2,3,4,5);;;/q;;3*+2/p-6</moldb-inchi>
  <moldb-inchikey>PRDPGWOYQAUJJB-UHFFFAOYSA-H</moldb-inchikey>
  <moldb-average-mass type="decimal">445.373</moldb-average-mass>
  <moldb-mono-mass type="decimal">445.607336209</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp nil="true"/>
  <hmdb-id nil="true"/>
  <chembl-id nil="true"/>
  <chemspider-id>23312</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference></synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM001137</chemdb-id>
  <dsstox-id nil="true"/>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00082107</susdat-id>
  <iupac nil="true"/>
  <moldb-polar-surface-area>86.25</moldb-polar-surface-area>
  <moldb-refractivity>5.7716</moldb-refractivity>
  <moldb-polarizability>6.298190073731611</moldb-polarizability>
  <moldb-rotatable-bond-count>0</moldb-rotatable-bond-count>
  <moldb-acceptor-count>4</moldb-acceptor-count>
  <moldb-donor-count>0</moldb-donor-count>
  <moldb-pka-strongest-acidic>3.153176570985763</moldb-pka-strongest-acidic>
  <moldb-pka-strongest-basic nil="true"/>
  <moldb-physiological-charge>-2</moldb-physiological-charge>
  <moldb-number-of-rings>0</moldb-number-of-rings>
  <moldb-alogps-logp nil="true"/>
  <moldb-alogps-logs nil="true"/>
  <moldb-alogps-solubility nil="true"/>
  <kingdom>Inorganic compounds</kingdom>
  <superklass>Mixed metal/non-metal compounds</superklass>
  <klass>Transition metal oxoanionic compounds</klass>
  <subklass>Transition metal arsenates</subklass>
  <paper-count type="integer">10</paper-count>
  <sync-id>CED0004086</sync-id>
  <structure-inchikey>PRDPGWOYQAUJJB-UHFFFAOYSA-H</structure-inchikey>
  <structure-fingerprint>24000000000000001000000000000000000000000000000000000000000000000000000000000200000000000000000000001000000000000000000000800000000000000000000000000000080000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000</structure-fingerprint>
  <structure-pattern-fingerprint>10000000010202008000000000002000000000000005000000200040800000044400000000800000000001000000000024200000000400000000443000a040008411040000000400000000000042000000300400000008020000002040000000082000020048000040000200c01000002000861000000004111800000010080200400008044000000800020000080000100400124000100000000800000000800040801000000000000008000024201002c00000000000001000001000000200800000a4048000020080000000000080000000000000400000000000080000000000001600000000000000010010000000000000004000000000000050000000</structure-pattern-fingerprint>
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AxogCgAAAAIDCCAiAAAA/wEhICAAAAAFCCAiAAAA/wEIICIAAAD/AQgAKAAA
AAMCCCAiAAAA/wEhICAAAAAFCCAiAAAA/wEIICIAAAD/AQgAKAAAAAMCCwME
AAQFAAQGAAQHCAIICQAJCgAJCwAJDAgCQgAAAAAXBAAAAAAAAAAW
</structure-pickle>
  <structure-indexed-at type="dateTime">2026-09-19T04:00:04Z</structure-indexed-at>
</compound>
