Zinc stearate (T3D0743)

IdentificationTaxonomyBiological PropertiesPhysical PropertiesToxicity ProfileSpectraConcentrationsLinksReferencesGene RegulationTargets (1)XML
Targets (1)
Record Information
Version2.0
Creation Date2009-03-27 01:41:44 UTC
Update Date2014-12-24 20:22:44 UTC
Accession NumberT3D0743
Identification
Common NameZinc stearate
ClassSmall Molecule
DescriptionZinc stearate is a chemical compound of zinc. It is used mainly as a releasing agent and lubricant in the rubber and plastics industry. Zinc is a metallic element with the atomic number 30. It is found in nature most often as the mineral sphalerite. Though excess zinc in harmful, in smaller amounts it is an essential element for life, as it is a cofactor for over 300 enzymes and is found in just as many transcription factors. (2, 3, 4)
Compound Type
  • Food Toxin
  • Household Toxin
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Organic Compound
  • Synthetic Compound
  • Zinc Compound
Chemical Structure
Thumb
MOLSDFPDBSMILESInChI
Synonyms
Synonym
Afco-chem ZNS
Antidust 2
Caswell No. 926
COAD
Dermarone
Dibasic zinc stearate
Hallcote ZS 5050
Hydense
Hytech
Mathe
Metallac
Metasap 576
Octadecanoic acid zinc salt, zinc octadecanoate
Octadecanoic acid, zinc salt
Octadecanoic acid, zinc salt (2:1)
Octadecanoic acid, zinc salt, basic
Petrac Zn-41
Stavinor ZN-e
Stearic acid zinc salt
Stearic acid, zinc salt
Synpro 8
Synpro stearate
Talculin z
Unichem ZS
Witco zinc stearate usp
Zinc dioctadecanoate
Zinc distearate
Zinc distearate, pure
Zinc octadecanoate
Zinc stearic acid
ZN stearate
Chemical FormulaC37H74O3Zn
Average Molecular Mass632.391 g/mol
Monoisotopic Mass630.493 g/mol
CAS Registry Number557-05-1
IUPAC Namezinc(2+) ion nonadecanoate octadecan-1-olate
Traditional Namezinc(2+) ion nonadecanoate octadecan-1-olate
SMILES[Zn++].CCCCCCCCCCCCCCCCCC[O-].CCCCCCCCCCCCCCCCCCC([O-])=O
InChI IdentifierInChI=1S/C19H38O2.C18H37O.Zn/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19(20)21;1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19;/h2-18H2,1H3,(H,20,21);2-18H2,1H3;/q;-1;+2/p-1
InChI KeyInChIKey=DRTRXJNQNGOVCT-UHFFFAOYSA-M
Chemical Taxonomy
Description belongs to the class of organic compounds known as long-chain fatty acids. These are fatty acids with an aliphatic tail that contains between 13 and 21 carbon atoms.
KingdomOrganic compounds
Super ClassLipids and lipid-like molecules
ClassFatty Acyls
Sub ClassFatty acids and conjugates
Direct ParentLong-chain fatty acids
Alternative Parents
Substituents
  • Long-chain fatty acid
  • Straight chain fatty acid
  • Carboxylic acid salt
  • Organic transition metal salt
  • Monocarboxylic acid or derivatives
  • Carboxylic acid
  • Carboxylic acid derivative
  • Organic oxygen compound
  • Organic oxide
  • Hydrocarbon derivative
  • Organic salt
  • Alkoxide
  • Organooxygen compound
  • Carbonyl group
  • Aliphatic acyclic compound
Molecular FrameworkNot Available
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Membrane
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point130°C
Boiling PointNot Available
SolubilityNot Available
LogPNot Available
Predicted Properties
PropertyValueSource
Water Solubility4.8e-06 g/LALOGPS
logP10.99ALOGPS
logP7.59ChemAxon
logS-8.1ALOGPS
pKa (Strongest Acidic)4.95ChemAxon
Physiological Charge-1ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area40.13 ŲChemAxon
Rotatable Bond Count33ChemAxon
Refractivity101.72 m³·mol⁻¹ChemAxon
Polarizability40.32 ųChemAxon
Number of Rings0ChemAxon
Bioavailability0ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
SpectraNot Available
Toxicity Profile
Route of ExposureInhalation (3) ; oral (3) ; dermal (3)
Mechanism of ToxicityAnaemia results from the excessive absorption of zinc suppressing copper and iron absorption, most likely through competitive binding of intestinal mucosal cells. Unbalanced levels of copper and zinc binding to Cu,Zn-superoxide dismutase has been linked to amyotrophic lateral sclerosis (ALS). Stomach acid dissolves metallic zinc to give corrosive zinc chloride, which can cause damage to the stomach lining. Metal fume fever is thought to be an immune response to inhaled zinc. (2, 3, 1)
MetabolismZinc can enter the body through the lungs, skin, and gastrointestinal tract. Intestinal absorption of zinc is controlled by zinc carrier protein CRIP. Zinc also binds to metallothioneins, which help prevent absorption of excess zinc. Zinc is widely distributed and found in all tissues and tissues fluids, concentrating in the liver, gastrointestinal tract, kidney, skin, lung, brain, heart, and pancreas. In the bloodstream zinc is found bound to carbonic anhydrase in erythrocytes, as well as bound to albumin, _2-macroglobulin, and amino acids in the the plasma. Albumin and amino acid bound zinc can diffuse across tissue membranes. Zinc is excreted in the urine and faeces. (3)
Toxicity ValuesLD50: >10000 mg/kg (Oral, Rat) (7) LD50: 354 mg/kg (Intraperitoneal, Mouse) (7)
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesZinc stearate is used mainly as a releasing agent and lubricant in the rubber and plastics industry. (4)
Minimum Risk LevelIntermediate Oral: 0.3 mg/kg/day (6) Chronic Oral: 0.3 mg/kg/day (6)
Health EffectsChronic exposure to zinc causes anemia, atazia, lethargy, and decreases the level of good cholesterol in the body. It is also believed to cause pancreatic and reproductive damage. (3)
SymptomsIngestion of large doses of zinc causes stomach cramps, nausea, and vomiting. Acute inhalation of large amounts of zinc causes metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Dermal contact with zinc results in skin irritation. (3)
TreatmentZinc poisoning is treated symptomatically, often by administering fluids such as water or milk, or with gastric lavage. (3)
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDNot Available
PubChem Compound ID11178
ChEMBL IDNot Available
ChemSpider ID30780121
KEGG IDNot Available
UniProt IDNot Available
OMIM ID
ChEBI IDNot Available
BioCyc IDNot Available
CTD IDNot Available
Stitch IDZinc stearate
PDB IDNot Available
ACToR ID3786
Wikipedia LinkNot Available
References
Synthesis ReferenceNot Available
MSDST3D0743.pdf
General References
  1. Vonk WI, Klomp LW: Role of transition metals in the pathogenesis of amyotrophic lateral sclerosis. Biochem Soc Trans. 2008 Dec;36(Pt 6):1322-8. doi: 10.1042/BST0361322. [19021549 ]
  2. Wikipedia. Zinc. Last Updated 24 March 2009. [Link]
  3. ATSDR - Agency for Toxic Substances and Disease Registry (2005). Toxicological profile for zinc. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  4. Wikipedia. Zinc stearate. Last Updated 3 February 2009. [Link]
  5. Wikipedia. Metallothionein. Last Updated 20 December 2008. [Link]
  6. ATSDR - Agency for Toxic Substances and Disease Registry (2001). Minimal Risk Levels (MRLs) for Hazardous Substances. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  7. The Physical and Theoretical Chemistry Laboratory of Oxford University (2005). Material Safety Data Sheet (MSDS) for zinc stearate. [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

Target Details
1. Superoxide dismutase [Cu-Zn]
General Function:
Zinc ion binding
Specific Function:
Destroys radicals which are normally produced within the cells and which are toxic to biological systems.
Gene Name:
SOD1
Uniprot ID:
P00441
Molecular Weight:
15935.685 Da
References
  1. Vonk WI, Klomp LW: Role of transition metals in the pathogenesis of amyotrophic lateral sclerosis. Biochem Soc Trans. 2008 Dec;36(Pt 6):1322-8. doi: 10.1042/BST0361322. [19021549 ]