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HCID 10431Erstellt: 27. Oktober 2026

Arsinous acid, As,As-dimethyl-, anhydride

TL-297 · Oxybis(dimethylarsine) · Bis(dimethylarsine) oxide · Bis(dimethylarsinous)anhydride · Arsinous acid, As,As-dimethyl-, anhydride

https://huagongshe.com/de/chemical/10431

Molekülstruktur von Arsinous acid, As,As-dimethyl-, anhydride

Identifikatoren & physikalische Daten

CAS No.	503-80-0
Summenformel	C4H12As2O
Durchschnittliche Molmasse	225,98 g/mol
Monoisotopische Masse	225,932 g/mol
SMILES	C[As](C)O[As](C)C
InChIKey	LOKPKYSOCCPWIZ-UHFFFAOYSA-N
PubChem CID	10431
DTXSID	DTXSID70198307

Chemische & physikalische Eigenschaften

Polarare Oberfläche (TPSA)	9,2
H-Brücken-Donoren	0
H-Brücken-Akzeptoren	1
Frei drehbare Bindungen	2
Schwere Atome	7
Formalladung	0
Komplexität	39
Schmelzpunkt	-25°C
Siedepunkt	150°C
Dichte	1.482
Brechungsindex	1.5225
Aggregatzustand	liquid

Sicherheit & Vorschriften

Minimum 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)
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)
Gesundheitliche Auswirkungen	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)
Expositionspfade	Oral (L2)inhalation (L2)dermal (L2)
Toxizitätsübersicht	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)
Signs and 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
Carcinogen Classification	3, not classifiable as to its carcinogenicity to humans. (L135)

CAS No.

503-80-0

Summenformel

C4H12As2O

Durchschnittliche Molmasse

225,98 g/mol

Monoisotopische Masse

225,932 g/mol

SMILES

C[As](C)O[As](C)C

InChIKey

LOKPKYSOCCPWIZ-UHFFFAOYSA-N

PubChem CID

10431

DTXSID

DTXSID70198307

Polarare Oberfläche (TPSA)

9,2

H-Brücken-Donoren

H-Brücken-Akzeptoren

Frei drehbare Bindungen

Schwere Atome

Formalladung

Komplexität

Schmelzpunkt

-25°C

Siedepunkt

150°C

Dichte

1.482

Brechungsindex

1.5225

Aggregatzustand

liquid

Sicherheit & Vorschriften

Minimum 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)

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)

Gesundheitliche Auswirkungen

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)

Expositionspfade

Oral (L2)inhalation (L2)dermal (L2)

Toxizitätsübersicht

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)

Signs and 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

Carcinogen Classification

3, not classifiable as to its carcinogenicity to humans. (L135)