ContaminantDB: Sodium cobaltinitrite

Identification Taxonomy Biological Properties Physical Properties Toxicity Profile Spectra Concentrations Links References Targets (44)XML

Record Information

Version

1.0

Creation Date

2009-03-22 21:52:41 UTC

Update Date

2016-11-09 01:08:19 UTC

Accession Number

CHEM000608

Identification

Common Name

Sodium cobaltinitrite

Class

Small Molecule

Description

Sodium cobaltinitrite is a chemical compound of cobalt. It is used as a qualitative test for potassium and ammonium ions. Cobalt is a metallic element with the atomic number 27. It is found naturally in rocks, soil, water, plants, and animals. In small amounts cobalt is an essential element for life, as it is part of vitamin B12. However, excess exposure is known to exhibit toxic effects. Nitrite is a toxic compound known to cause methemoglobinemia. (8, 3, 4, 5)

Contaminant Sources

T3DB toxins

Contaminant Type

Cobalt Compound
Industrial/Workplace Toxin
Inorganic Compound
Nitrite
Pollutant
Synthetic Compound

Chemical Structure

MOL SDF PDB SMILES InChI

Synonyms

Not Available

Chemical Formula

CoH₆N₆Na₃O₁₂

Average Molecular Mass

409.983 g/mol

Monoisotopic Mass

409.907 g/mol

CAS Registry Number

13600-98-1

IUPAC Name

cobalt(3+) ion trisodium hexakis(nitrous acid)

Traditional Name

cobalt(3+) ion trisodium hexakis(nitrous acid)

SMILES

[Na+].[Na+].[Na+].[Co+3].ON=O.ON=O.ON=O.ON=O.ON=O.ON=O

InChI Identifier

InChI=1S/Co.6HNO2.3Na/c;6*2-1-3;;;/h;6*(H,2,3);;;/q+3;;;;;;;3*+1

InChI Key

ZEBNDJQGEZXBCR-UHFFFAOYSA-N

Chemical Taxonomy

Description

belongs to the class of inorganic compounds known as transition metal nitrites. These are inorganic compounds in which the largest oxoanion is nitrite, and in which the heaviest atom not in an oxoanion is a transition metal.

Kingdom

Inorganic compounds

Super Class

Mixed metal/non-metal compounds

Class

Transition metal oxoanionic compounds

Sub Class

Transition metal nitrites

Direct Parent

Transition metal nitrites

Alternative Parents

Substituents

Transition metal nitrite
Inorganic nitrite
Inorganic cobalt salt
Inorganic oxide
Inorganic salt

Molecular Framework

Not Available

External Descriptors

Not Available

Biological Properties

Status

Detected and Not Quantified

Origin

Exogenous

Cellular Locations

Cytoplasm
Extracellular

Biofluid Locations

Not Available

Tissue Locations

Not Available

Pathways

Not Available

Applications

Not Available

Biological Roles

Not Available

Chemical Roles

Not Available

Physical Properties

State

Solid

Appearance

Yellow solid.

Experimental Properties

Property	Value
Melting Point	Not Available
Boiling Point	Not Available
Solubility	Not Available

Predicted Properties

Property	Value	Source
logP	0.17	ChemAxon
pKa (Strongest Acidic)	3.32	ChemAxon
pKa (Strongest Basic)	-3.5	ChemAxon
Physiological Charge	-1	ChemAxon
Hydrogen Acceptor Count	3	ChemAxon
Hydrogen Donor Count	1	ChemAxon
Polar Surface Area	49.66 Å²	ChemAxon
Rotatable Bond Count	0	ChemAxon
Refractivity	8.72 m³·mol⁻¹	ChemAxon
Polarizability	2.81 Å³	ChemAxon
Number of Rings	0	ChemAxon
Bioavailability	1	ChemAxon
Rule of Five	Yes	ChemAxon
Ghose Filter	No	ChemAxon
Veber's Rule	No	ChemAxon
MDDR-like Rule	No	ChemAxon

Spectra

Not Available

Toxicity Profile

Route of Exposure

Inhalation (3) ; oral (3) ; dermal (3)

Mechanism of Toxicity

Cobalt is believed to exhibit its toxicity through a oxidant-based and free radical-based processes. It produces oxygen radicals and may be oxidized to ionic cobalt, causing increased lipid peroxidation, DNA damage, and inducing certain enzymes that lead to cell apoptosis. Cobalt has also been shown to block inorganic calcium channels, possibly impairing neurotransmission. Cobalt can also chelate lipoic acids, impairing oxidation of pyruvate or fatty acids. In addition, cobalt may inhibit DNA repair by interacting with zinc finger DNA repair proteins, and has also been shown to inhibit heme synthesis and glucose metabolism. Cobalt may activate specific helper T-lymphocyte cells and interact directly with immunologic proteins, such as antibodies (IgA and IgE) or Fc receptors, resulting in immunosensitization. (3) Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (2, 9)

Metabolism

Cobalt is absorbed though the lungs, gastrointestinal tract, and skin. Since it is a component of the vitamin B12 (cyanocobalamin), it is distributed to most tissues of the body. It is transported in the blood, often bound to albumin, with the highest levels being found in the liver and kidney. Cobalt is excreted mainly in the urine and faeces. Nitrites and their metabolites are also excreted in the urine. (8, 3)

Toxicity Values

Not Available

Lethal Dose

10 to 100 mg/kg for an adult human. (10)

Carcinogenicity (IARC Classification)

Ingested nitrate or nitrite under conditions that result in endogenous nitrosation is probably carcinogenic to humans (Group 2A). Cobalt compounds are possibly carcinogenic to humans (Group 2B).

Uses/Sources

Sodium cobaltinitrite is used as a qualitative test for potassium and ammonium ions. (5)

Minimum Risk Level

Chronic Inhalation: 0.0001 mg/m3 (6) Intermediate Oral: 0.01 mg/kg/day (6)

Health Effects

Exposure to high amount of cobalt can cause heart, lung, kidney, and liver damage. Skin contact is known to result in contact dermatitus. Cobalt may also have mutagenic and carcinogenic effects. Nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (8, 3, 4)

Symptoms

Cobalt inhalation can cause asthma-like breathing problems. Skin contact is known to result in contact dermatitis, which is characterized by irritation and rashes. Ingesting large amounts of cobalt may cause nausea and vomiting. Nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (11, 8, 3)

Treatment

Treatment of cobalt poisoning is symptomatic. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (9, 3)

Concentrations

Not Available

External Links

DrugBank ID

Not Available

HMDB ID

Not Available

FooDB ID

Not Available

Phenol Explorer ID

Not Available

KNApSAcK ID

Not Available

BiGG ID

Not Available

BioCyc ID

Not Available

METLIN ID

Not Available

PDB ID

Not Available

Wikipedia Link

Sodium cobaltinitrite

Chemspider ID

Not Available

ChEBI ID

Not Available

PubChem Compound ID

44134942

Kegg Compound ID

Not Available

YMDB ID

Not Available

ECMDB ID

Not Available

References

Synthesis Reference

Not Available

MSDS

Not Available

General References

Not Available

Sodium cobaltinitrite (CHEM000608)

Structure for CHEM000608: Sodium cobaltinitrite