o-Phenylenbis(dimethylarsin)

Diars · Phenylenebisdimethylarsine · O-PHENYLENEBISDIMETHYLARSINE · 2-phenylene-bis-dimethylarsine · 1,2-Bis(dimethylarsino)benzene · 1,2-phenylenebis(dimethylarsane) · 1,2-Phenylenebis(dimethylarsine) · 1,2-Benzenediylbis(dimethylarsine)

https://huagongshe.com/de/chemical/83261

Molekülstruktur von o-Phenylenbis(dimethylarsin)

Identifikatoren & physikalische Daten

CAS No.	13246-32-7
Summenformel	C10H16As2
Durchschnittliche Molmasse	286,08 g/mol
Monoisotopische Masse	285,96839 g/mol
SMILES	C[As](C)c1ccccc1[As](C)C
InChIKey	HUBWRAMPQVYBRS-UHFFFAOYSA-N
PubChem CID	83261
ChEBI	CHEBI:30628
EC No.	236-227-9
DTXSID	DTXSID50157593
Lokaler Name	o-Phenylenbis(dimethylarsin)

Chemische & physikalische Eigenschaften

Polarare Oberfläche (TPSA)	0
H-Brücken-Donoren	0
H-Brücken-Akzeptoren	0
Frei drehbare Bindungen	2
Schwere Atome	12
Formalladung	0
Komplexität	116

Sicherheit & Vorschriften

Regulatorische Informationen	Restricted substance: o-phenylenebis(dimethylarsine)
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.

13246-32-7

Summenformel

C10H16As2

Durchschnittliche Molmasse

286,08 g/mol

Monoisotopische Masse

285,96839 g/mol

SMILES

C[As](C)c1ccccc1[As](C)C

InChIKey

HUBWRAMPQVYBRS-UHFFFAOYSA-N

PubChem CID

83261

ChEBI

CHEBI:30628

EC No.

236-227-9

DTXSID

DTXSID50157593

Lokaler Name

o-Phenylenbis(dimethylarsin)

Polarare Oberfläche (TPSA)

H-Brücken-Donoren

H-Brücken-Akzeptoren

Frei drehbare Bindungen

Schwere Atome

Formalladung

Komplexität

116

Sicherheit & Vorschriften

Regulatorische Informationen

Restricted substance: o-phenylenebis(dimethylarsine)

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)