Manganese selenide (MnSe2)

https://huagongshe.com/de/chemical/83014

Identifikatoren & physikalische Daten

CAS No.	12299-98-8
Summenformel	MnSe2
Durchschnittliche Molmasse	212,88 g/mol
Monoisotopische Masse	214,77109 g/mol
SMILES	[Se]=[Mn]=[Se]
InChIKey	KDAKOPXAEMJUSU-UHFFFAOYSA-N
PubChem CID	83014
EC No.	235-569-6
DTXSID	DTXSID0065301

Chemische & physikalische Eigenschaften

Polarare Oberfläche (TPSA)	0
H-Brücken-Donoren	0
H-Brücken-Akzeptoren	0
Frei drehbare Bindungen	0
Schwere Atome	3
Formalladung	0
Komplexität	18,3
SpringerMaterials Properties	crystal structure

Sicherheit & Vorschriften

Minimum Risk Level	Chronic Inhalation: 0.0003 mg/m3 (Manganese) (L134) Chronic Oral: 0.005 mg/kg/day (Selenium) (L134)
Treatment	EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.
Gesundheitliche Auswirkungen	Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228)
Expositionspfade	Oral (L619)inhalation (L619)dermal (L619)
Toxizitätsübersicht	Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to perturbations other neurotransmitters, such as GABA and glutamate. In order to produce oxidative damage, manganese must first overwhelm the antioxidant enzyme manganese superoxide dismutase. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619, L228)
Signs and Symptoms	Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228)
Carcinogen Classification	3, not classifiable as to its carcinogenicity to humans. (L135)

CAS No.

12299-98-8

Summenformel

MnSe2

Durchschnittliche Molmasse

212,88 g/mol

Monoisotopische Masse

214,77109 g/mol

SMILES

[Se]=[Mn]=[Se]

InChIKey

KDAKOPXAEMJUSU-UHFFFAOYSA-N

PubChem CID

83014

EC No.

235-569-6

DTXSID

DTXSID0065301

Polarare Oberfläche (TPSA)

H-Brücken-Donoren

H-Brücken-Akzeptoren

Frei drehbare Bindungen

Schwere Atome

Formalladung

Komplexität

18,3

SpringerMaterials Properties

crystal structure

Sicherheit & Vorschriften

Minimum Risk Level

Chronic Inhalation: 0.0003 mg/m3 (Manganese) (L134) Chronic Oral: 0.005 mg/kg/day (Selenium) (L134)

Treatment

EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.

Gesundheitliche Auswirkungen

Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228)

Expositionspfade

Oral (L619)inhalation (L619)dermal (L619)

Toxizitätsübersicht

Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to perturbations other neurotransmitters, such as GABA and glutamate. In order to produce oxidative damage, manganese must first overwhelm the antioxidant enzyme manganese superoxide dismutase. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619, L228)

Signs and Symptoms

Carcinogen Classification

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