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Record Information
Creation Date2009-03-06 18:58:27 UTC
Update Date2016-11-09 01:08:12 UTC
Accession NumberCHEM000241
Common NameCopper arsenate
ClassSmall Molecule
DescriptionCopper arsenate is a chemical compound of copper and arsenic. It is derived from arsenic acid and used mainly as a pesticide. Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential elements in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. Arsenic is a chemical element that has the symbol As and atomic number 33. It is a poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenopyrite and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as a compound with other elements. (5, 13, 14, 17)
Contaminant Sources
  • IARC Carcinogens Group 1
  • T3DB toxins
Contaminant Type
  • Arsenic Compound
  • Copper Compound
  • Inorganic Compound
  • Metalloid
  • Pesticide
  • Pollutant
  • Synthetic Compound
Chemical Structure
Copper arsenic acidGenerator
Chemical FormulaAs2Cu3O8
Average Molecular Mass468.476 g/mol
Monoisotopic Mass466.591 g/mol
CAS Registry Number10103-61-4
IUPAC Nametricopper(2+) ion diarsorate
Traditional Nametricopper(2+) ion diarsenate
InChI IdentifierInChI=1S/2AsH3O4.3Cu/c2*2-1(3,4)5;;;/h2*(H3,2,3,4,5);;;/q;;3*+2/p-6
Chemical Taxonomy
Description belongs to the class of inorganic compounds known as transition metal arsenates. These are inorganic compounds in which the largest oxoanion is arsenate, and in which the heaviest atom not in an oxoanion is a transition metal.
KingdomInorganic compounds
Super ClassMixed metal/non-metal compounds
ClassTransition metal oxoanionic compounds
Sub ClassTransition metal arsenates
Direct ParentTransition metal arsenates
Alternative Parents
  • Transition metal arsenate
  • Arsenate
  • Inorganic copper salt
  • Inorganic oxide
  • Inorganic salt
  • Inorganic metalloid salt
  • Inorganic arsenic compound
Molecular FrameworkNot Available
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
Cellular Locations
  • Cytoplasm
  • Extracellular
  • Microtubule
  • Mitochondrion
  • Plasma Membrane
  • Soluble Fraction
  • Tubulin
Biofluid LocationsNot Available
Tissue LocationsNot Available
EicosanoidsNot AvailableNot Available
Oxidative phosphorylationNot Availablemap00190
Biosynthesis Of Amino AcidsNot AvailableNot Available
ApoptosisNot Availablemap04210
Abc transportersNot Availablemap02010
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
AppearanceBlue-green powder.
Experimental Properties
Melting Point1100°C
Boiling PointNot Available
SolubilityNot Available
Predicted Properties
Water Solubility47.6 g/LALOGPS
pKa (Strongest Acidic)3.15ChemAxon
Physiological Charge-2ChemAxon
Hydrogen Acceptor Count4ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area86.25 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity5.77 m³·mol⁻¹ChemAxon
Polarizability6.3 ųChemAxon
Number of Rings0ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
SpectraNot Available
Toxicity Profile
Route of ExposureOral (8) ; inhalation (8); dermal (8)
Mechanism of ToxicityExcess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. 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. (4, 1, 13, 7, 2, 16)
MetabolismCopper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. 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. (9, 13, 15)
Toxicity ValuesLD50: 2147 mg/kg (Oral, Rat) (18)
Lethal Dose10 to 20 grams for an adult human (copper salts). (6)
Carcinogenicity (IARC Classification)1, carcinogenic to humans. (12)
Uses/SourcesCopper arsenate is used as an insecticide, herbicide, fungicide, and rodenticide. (17)
Minimum Risk LevelAcute Oral: 0.01 mg/kg/day (Copper) (11) Intermediate Oral: 0.01 mg/kg/day (Copper) (11) Acute Oral: 0.005 mg/kg/day (Arsenic) (11) Chronic Oral: 0.0003 mg/kg/day (Arsenic) (11) Chronic Inhalation: 0.01 mg/m3 (Arsenic) (11)
Health EffectsPeople must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. 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. (4, 9, 14, 15)
SymptomsBreathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. 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 burn (4).
TreatmentArsenic 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. (9)
Not Available
DrugBank IDNot Available
HMDB IDNot Available
FooDB IDNot Available
Phenol Explorer IDNot Available
KNApSAcK IDNot Available
BiGG IDNot Available
BioCyc IDNot Available
METLIN IDNot Available
PDB IDNot Available
Wikipedia LinkCopper(II) arsenate
Chemspider IDNot Available
ChEBI IDNot Available
PubChem Compound ID26065
Kegg Compound IDNot Available
YMDB IDNot Available
ECMDB IDNot Available
Synthesis ReferenceNot Available
MSDSNot Available
General ReferencesNot Available