Arsenic (CED0000001)

Record Information

Version

1.0

Creation Date

2009-03-06 18:57:53 UTC

Update Date

2026-04-06 04:23:41 UTC

Accession Number

CHEM000001

Identification

Common Name

Arsenic

Class

Small Molecule

Description

Arsenic (As) is a solid at room temperature with an average molecular weight of 74.92 g/mol. Arsenic belongs to the homogeneous metalloid compounds, a class of homogeneous metal compounds within the inorganic compounds. This exogenous compound is used as a biological micronutrient and is identified as an industrial degradant or impurity. It is present in polystyrene and used in polyurethane and low-density polyethylene, while it is released from polycarbonate, polyethylene terephthalate, polyvinyl chloride, and polypropylene. Recorded sources of arsenic include food contact materials, tobacco product cases, pipe accessories, and electrical and electronic equipment such as discharge lamps, antennas, cores yokes or armatures, and amplifiers. Exposure occurs via touch, oral, and inhalation routes. Arsenic is associated with cancer (PMC11991570). It binds to various protein targets, including the estrogen receptor, glucocorticoid receptor, hemoglobin subunit alpha (HBA1), hemoglobin subunit beta (HBB), haptoglobin, and kelch-like ECH-associated protein 1. Binding to glutathione reductase (GSR) results in the inhibition of essential biochemical reactions, alteration of cellular redox status, and eventual cytotoxicity. Binding to PARP-1 is believed to induce carcinogenesis by affecting DNA repair. Additionally, arsenic disrupts ATP production by competing with phosphate to uncouple oxidative phosphorylation and inhibiting pyruvate dehydrogenase at the level of the citric acid cycle, which inhibits mitochondrial respiration, energy-linked reduction of NAD+, and ATP synthesis. This process increases hydrogen peroxide production, which may form oxidative stress and reactive oxygen species. Targeted proteins in the pyruvate dehydrogenase complex include PDHB, PDHA1, DLAT, and the testis-specific form PDHA2.

Contaminant Type

Arsenic Compound
Cigarette Toxin
Food Toxin
Household Toxin
Human Neurotoxin
Inorganic Compound
Metabolite
Metal
Metalloid
Natural Compound
Pesticide
Pollutant

Chemical Structure

MOL SDF PDB SMILES InChI

Synonyms

Value	Source
As(3+)	ChEBI
Arsen	HMDB
Arsenic black	HMDB
Arsenic elemental	HMDB
As	HMDB
Grey arsenic	HMDB
Metallic arsenic	HMDB

Chemical Formula

Average Molecular Mass

74.922 g/mol

Monoisotopic Mass

74.922 g/mol

CAS Registry Number

7440-38-2

IUPAC Name

arsenic(3+) ion

Traditional Name

arsenic(3+) ion

SMILES

[As+3]

InChI Identifier

InChI=1S/As/q+3

InChI Key

LULLIKNODDLMDQ-UHFFFAOYSA-N

Chemical Taxonomy

Description

Belongs to the class of inorganic compounds known as homogeneous metalloid compounds. These are inorganic compounds containing only metal atoms,with the largest atom being a metalloid atom.

Kingdom

Inorganic compounds

Super Class

Homogeneous metal compounds

Class

Homogeneous metalloid compounds

Sub Class

Not Available

Direct Parent

Homogeneous metalloid compounds

Alternative Parents

Not Available

Substituents

Homogeneous metalloid

Molecular Framework

Not Available

External Descriptors

monoatomic arsenic (CHEBI:35828 )

Biological Properties

Status

Detected and Not Quantified

Origin

Exogenous

Cellular Locations

Cytoplasm
Extracellular

Biofluid Locations

Not Available

Tissue Locations

Not Available

Applications

Not Available

Biological Roles

micronutrient

Chemical Roles

Not Available

Organoleptic Effects

Not Available

Physical Properties

State

Solid

Appearance

Grey metallic solid.

Experimental Properties

Property	Value
Melting Point	> 615°C
Boiling Point	614 °C
Solubility	Not Available

Predicted Properties

Property	Value	Source
logP	0.75	ChemAxon
Physiological Charge	3	ChemAxon
Hydrogen Acceptor Count	0	ChemAxon
Hydrogen Donor Count	0	ChemAxon
Polar Surface Area	0 Å²	ChemAxon
Rotatable Bond Count	0	ChemAxon
Refractivity	0 m³·mol⁻¹	ChemAxon
Polarizability	1.78 Å³	ChemAxon
Number of Rings	0	ChemAxon
Bioavailability	Yes	ChemAxon
Rule of Five	Yes	ChemAxon
Ghose Filter	No	ChemAxon
Veber's Rule	Yes	ChemAxon
MDDR-like Rule	No	ChemAxon

Spectra

Spectrum Type	Description	Splash Key	Deposition Date	View
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum	splash10-001i-9000000000-6183cd0482f342082392	Not Available	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum	splash10-001i-9000000000-6183cd0482f342082392	Not Available	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum	splash10-001i-9000000000-6183cd0482f342082392	Not Available	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum	splash10-004i-9000000000-30fac8ea879bd5e34966	Not Available	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum	splash10-004i-9000000000-30fac8ea879bd5e34966	Not Available	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum	splash10-004i-9000000000-30fac8ea879bd5e34966	Not Available	View Spectrum

Toxicity Profile

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 carcinogenicity 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. (12, 4)

Carcinogenicity (IARC Classification)

1, carcinogenic to humans. (11)

Minimum Risk Level

Acute Oral: 0.005 mg/kg/day (10) Chronic Oral: 0.0003 mg/kg/day (10) Chronic Inhalation: 0.01 mg/m3 (10) The World Health Organization asserts that a level of 0.01 mg/L in drinking water poses a risk of 1/1600 chance of lifetime skin cancer risk.

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 “pins and needles” in hands and feet. Breathing high levels of inorganic arsenic can give you a sore throat or irritated lungs. Arsenic also affects the brain, causing neurological disturbances such as headaches, confusion, and drowsiness. (1)

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. (8)

Toxicity Values

Toxicity Value	Unit	Value Range	Organism	Dose Descriptor	Route of Exposure	Predicted or Experimental	Reference
763.0	mg/kg	Not Available	Rat	LD50	Oral	experimental	T14
13.4	ug/kg	Not Available	Rat	LD50	Intraperitoneal	experimental	T14

Health Effects

Health Effect	Relationship	Direction	Reference
cancer	associated_with	Not Available	PMC11991570

Exposure Sources

Source ID	Source	Sector	Reference
494	Food contact materials	Food, food processing & cookware	Not Available
505	Amplifiers	Electrical & Electronic Equipment	Not Available
506	Antennas	Electrical & Electronic Equipment	Not Available
513	Cores Yokes Or Armatures	Electrical & Electronic Equipment	Not Available
514	Discharge Lamps	Electrical & Electronic Equipment	Not Available
562	Pipe Accessories	Household cleaning & consumer products	Not Available
567	Tobacco Product Cases	Household cleaning & consumer products	Not Available
579	Manufacture Of Iron Or Steel	Industrial manufacturing & chemical processing	Not Available

Pathways

0 pathways

No pathways found

No metabolic pathways have been associated with this synthetic chemical

Targets

Structure	Protein	UniProt ID	Organism	Relationship	Details
Click to view 3D structure	Tubulin beta chain	P07437	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Actin, alpha skeletal muscle	P68133	Humans	Known	Arsenic binds to actin. (A16)
Click to view 3D structure	Actin, aortic smooth muscle	P62736	Humans	Known	Arsenic binds to actin. (A16)
Click to view 3D structure	Actin, cytoplasmic 1	P60709	Humans	Known	Arsenic binds to actin. (A16)
Click to view 3D structure	Actin, cytoplasmic 2	P63261	Humans	Known	Arsenic binds to actin. (A16)
Click to view 3D structure	Dihydrolipoyllysine-residue acetyltransferase component of pyruvate dehydrogenase complex, mitochondrial	P10515	Humans	Known	Arsenic disrupts 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. (T1)
Click to view 3D structure	Estrogen receptor	P03372	Humans	Known	Arsenic binds to the estrogen receptor. (A17)
Click to view 3D structure	Glucocorticoid receptor	P04150	Humans	Known	Arsenic binds to the glucocorticoid receptor. (A17)
Click to view 3D structure	Glutathione reductase, mitochondrial	P00390	Humans	Known	Arsenic binds glutathione reductase, which results in the inhibition of essential biochemical reactions, alteration of cellular redox status, and eventual cytotoxicity. (L2)
Click to view 3D structure	Hemoglobin subunit alpha	P69905	Humans	Known	Arsenic binds to hemoglobin. (A15)
Click to view 3D structure	Hemoglobin subunit beta	P68871	Humans	Known	Arsenic binds to hemoglobin. (A15)
Click to view 3D structure	Kelch-like ECH-associated protein 1	Q14145	Humans	Known	Arsenic binds to kelch-like ECH-associated protein 1. (A17)
Click to view 3D structure	Metallothionein-1A	P04731	Humans	Known	Not Available
Click to view 3D structure	Poly [ADP-ribose] polymerase 1	P09874	Humans	Known	Arsenic binding of PARP-1 is believed to induce carcinogenesis by affecting DNA repair. (A17)
Click to view 3D structure	Tubulin-like protein alpha-4B	Q9H853	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Pyruvate dehydrogenase E1 component subunit alpha, somatic form, mitochondrial	P08559	Humans	Known	Arsenic disrupts 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. (T1)
Click to view 3D structure	Pyruvate dehydrogenase E1 component subunit alpha, testis-specific form, mitochondrial	P29803	Humans	Known	Arsenic disrupts 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. (T1)
Click to view 3D structure	Pyruvate dehydrogenase E1 component subunit beta, mitochondrial	P11177	Humans	Known	Arsenic disrupts 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. (T1)
Click to view 3D structure	Pyruvate kinase PKM	P14618	Humans	Known	Not Available
Click to view 3D structure	Thioredoxin reductase 1, cytoplasmic	Q16881	Humans	Known	Arsenic binds thioredoxin reductase, which results in the inhibition of essential biochemical reactions, alteration of cellular redox status, and eventual cytotoxicity. (L2)
Click to view 3D structure	Thioredoxin reductase 2, mitochondrial	Q9NNW7	Humans	Known	Arsenic binds thioredoxin reductase, which results in the inhibition of essential biochemical reactions, alteration of cellular redox status, and eventual cytotoxicity. (L2)
Click to view 3D structure	Tubulin alpha-1A chain	Q71U36	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin alpha-1B chain	P68363	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin alpha-1C chain	Q9BQE3	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin alpha-3E chain	Q6PEY2	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin alpha-4A chain	P68366	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin alpha-8 chain	Q9NY65	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-1 chain	Q9H4B7	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-2A chain	Q13885	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-2B chain	Q9BVA1	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-3 chain	Q13509	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-4A chain	P04350	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-4B chain	P68371	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)
Click to view 3D structure	Tubulin beta-6 chain	Q9BUF5	Humans	Known	Arsenic's carginogenicity is believed to be caused by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. (A17)