Record Information
Version1.0
Creation Date2009-03-06 18:58:06 UTC
Update Date2026-05-14 18:23:42 UTC
Accession NumberCHEM000108
Identification
Common NameManganese
ClassSmall Molecule
DescriptionManganese is an essential trace nutrient in all forms of life. Physiologically, it. exists as an ion in the body. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver.
Contaminant Sources
  • Clean Air Act Chemicals
  • FooDB Chemicals
  • HMDB Contaminants - Urine
  • HPV EPA Chemicals
  • T3DB toxins
Contaminant Type
  • Cosmetic Toxin
  • Food Toxin
  • Household Toxin
  • Human Neurotoxin
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Manganese Compound
  • Metabolite
  • Metal
  • Natural Compound
  • Pollutant
Chemical Structure
Thumb
Synonyms
ValueSource
MANGANESE (II) ionChEBI
Manganese(II)ChEBI
Manganese, ion (MN2+)ChEBI
Manganous ionChEBI
MN(II)ChEBI
MN(2+)ChEBI
MN2+ChEBI
Chemical FormulaMn
Average Molecular Mass54.938 g/mol
Monoisotopic Mass54.938 g/mol
CAS Registry Number7439-96-5
IUPAC Namemanganese(2+) ion
Traditional Namemanganese(2+) ion
SMILES[Mn++]
InChI IdentifierInChI=1S/Mn/q+2
InChI KeyWAEMQWOKJMHJLA-UHFFFAOYSA-N
Chemical Taxonomy
Description belongs to the class of inorganic compounds known as homogeneous transition metal compounds. These are inorganic compounds containing only metal atoms,with the largest atom being a transition metal atom.
KingdomInorganic compounds
Super ClassHomogeneous metal compounds
ClassHomogeneous transition metal compounds
Sub ClassNot Available
Direct ParentHomogeneous transition metal compounds
Alternative ParentsNot Available
Substituents
  • Homogeneous transition metal
Molecular FrameworkNot Available
External Descriptors
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue Locations
  • Basal Ganglia
  • Brain
  • Central Nervous System
  • Hair
  • Liver
PathwaysNot Available
ApplicationsNot Available
Biological Roles
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point1244°C
Boiling Point2095°C (3803°F)
SolubilityNot Available
Predicted Properties
PropertyValueSource
logP-0.16ChemAxon
pKa (Strongest Acidic)3.09ChemAxon
Physiological Charge2ChemAxon
Hydrogen Acceptor Count0ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area0 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity0 m³·mol⁻¹ChemAxon
Polarizability1.78 ųChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterNoChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleNoChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyView
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-0a4i-9000000000-6f3891a406ae3fe4f883Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-0a4i-9000000000-6f3891a406ae3fe4f883Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-0a4i-9000000000-6f3891a406ae3fe4f883Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-0udi-9000000000-c3110d268939143a5f80Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-0udi-9000000000-c3110d268939143a5f80Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0udi-9000000000-c3110d268939143a5f80Spectrum
Toxicity Profile
Route of ExposureOral (22) ; inhalation (22)
Mechanism of ToxicityManganese 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 interact with other neurotransmitters, such as GABA and glutamate. Manganese overwhelms the manganese superoxide dismutase and produce oxidative damage. 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. (22)
MetabolismManganese is mainly absorbed via ingestion, but can also be inhaled. It binds to alpha-2-macroglobulin, albumin, or transferrin in the plasma and is distributed to the brain and all other mammalian tissues, though it tends to accumulate more in the liver, pancreas, and kidney. Manganese exists in a number of oxidation states and is believed to undergo changes in oxidation state within the body. Manganese oxidation state can influence tissue toxicokinetic behavior, and possibly toxicity. Manganese is excreted primarily in the faeces. (22)
Toxicity ValuesLD50: 9 g/kg (Oral, Rat) (24)
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesManganese is used principally in steel production to improve hardness, stiffness, and strength. It may also be used as an additive in gasoline to improve the octane rating of the gas. Manganese ions have various colors and are used industrially as pigments. (22, 23)
Minimum Risk LevelChronic Inhalation: 0.0003 mg/m3 (21)
Health EffectsManganese 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”. High levels of manganese may also cause damage to the reproductive system. (22)
SymptomsManganese 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”. (22)
TreatmentNot Available
Concentrations
Not Available
DrugBank IDDB06757
HMDB IDHMDB0001333
FooDB IDFDB031005
Phenol Explorer IDNot Available
KNApSAcK IDNot Available
BiGG IDNot Available
BioCyc IDNot Available
METLIN IDNot Available
PDB IDNot Available
Wikipedia LinkManganese
Chemspider ID25916
ChEBI ID29035
PubChem Compound ID27854
Kegg Compound IDC19610
YMDB IDYMDB01521
ECMDB IDECMDB01333
References
Synthesis ReferenceNot Available
MSDSLink
General References
1. Raghib MH, Chan WY, Rennert OM: Comparative biological availability of manganese from extrinsically labelled milk diets using sucking rats as a model. Br J Nutr. 1986 Jan;55(1):49-58.
2. A. PECHOVÁ et al. Contents of Zn, Cu, Mn and Se in Milk in Relation to their Concentrations in Blood, Milk Yield and Stage of Lactation in Dairy Cattle. Acta Vet. Brno 2008, 77: 523-531
3. Semaghiul Birghila, Simona Dobrinas, Gabriela Stanciu and Alina Soceanu. Determination of major and minor elements in milk through ICP-AES. Environmental Engineering and Management Journal. November/December 2008, Vol.7, No.6, 805-808
4. Park, Y. W; Juárez, Manuela ; Ramos, M.; Haenlein, G. F. W.. Physico-chemical characteristics of goat and sheep milk. Small Ruminant Res.(2007) 68:88-113 doi: 10.1016/j.smallrumres.2006.09.013
5. A. Foroutan et al. The Chemical Composition of Commercial Cow's Milk (in preparation)
6. Patricia Cava-Montesinos, M. Luisa Cervera Agustín Pastor Miguel de la Guardia. 2005. Room temperature acid sonication ICP-MS multielemental analysis of milk.Analytica Chimica Acta Volume 531, Issue 1, Pages 111-123
7. Z. Dobrzański, R. Kołacz, H. Górecka, K. Chojnacka, A. Bartkowiak. 2005. The Content of Microelements and Trace Elements in Raw Milk from Cows in the Silesian Region. Pol. J. Environ. Stud. 14(5):685–689
8. Fooddata+, The Technical University of Denmark (DTU): https://frida.fooddata.dk/QueryFood.php?fn=milk&lang=en
9. Ikeda S, Sera Y, Yoshida M, Ohshiro H, Uchino S, Oka Y, Lee KJ, Kotera A: Manganese deposits in patients with biliary atresia after hepatic porto-enterostomy. J Pediatr Surg. 2000 Mar;35(3):450-3.
10. Greger JL: Nutrition versus toxicology of manganese in humans: evaluation of potential biomarkers. Neurotoxicology. 1999 Apr-Jun;20(2-3):205-12.
11. Lander F, Kristiansen J, Lauritsen JM: Manganese exposure in foundry furnacemen and scrap recycling workers. Int Arch Occup Environ Health. 1999 Nov;72(8):546-50.
12. Mizoguchi N, Nishimura Y, Ono H, Sakura N: Manganese elevations in blood of children with congenital portosystemic shunts. Eur J Pediatr. 2001 Apr;160(4):247-50.
13. Woolf A, Wright R, Amarasiriwardena C, Bellinger D: A child with chronic manganese exposure from drinking water. Environ Health Perspect. 2002 Jun;110(6):613-6.
14. Ikeda S, Yamaguchi Y, Sera Y, Ohshiro H, Uchino S, Yamashita Y, Ogawa M: Manganese deposition in the globus pallidus in patients with biliary atresia. Transplantation. 2000 Jun 15;69(11):2339-43.
15. Wardle CA, Forbes A, Roberts NB, Jawhari AV, Shenkin A: Hypermanganesemia in long-term intravenous nutrition and chronic liver disease. JPEN J Parenter Enteral Nutr. 1999 Nov-Dec;23(6):350-5.
16. Mergler D, Baldwin M, Belanger S, Larribe F, Beuter A, Bowler R, Panisset M, Edwards R, de Geoffroy A, Sassine MP, Hudnell K: Manganese neurotoxicity, a continuum of dysfunction: results from a community based study. Neurotoxicology. 1999 Apr-Jun;20(2-3):327-42.
17. Butterworth RF: Hepatic encephalopathy. Alcohol Res Health. 2003;27(3):240-6.
18. Herynek V, Babis M, Trunecka P, Filip K, Vymazal J, Dezortova M, Hajek M: Chronic liver disease: relaxometry in the brain after liver transplantation. MAGMA. 2001 Mar;12(1):10-5.
19. Miranda M, Caballero L: [Chronic hepatic encephalopathy: the role of high serum manganese levels and its relation with basal ganglia lesions in nuclear magnetic resonance of the brain. Clinical case]. Rev Med Chil. 2001 Sep;129(9):1051-5.
20. Barceloux DG: Manganese. J Toxicol Clin Toxicol. 1999;37(2):293-307.
21. Bader M, Dietz MC, Ihrig A, Triebig G: Biomonitoring of manganese in blood, urine and axillary hair following low-dose exposure during the manufacture of dry cell batteries. Int Arch Occup Environ Health. 1999 Nov;72(8):521-7.
22. Kao HJ, Chen WH, Liu JS: Rapid progression of parkinsonism associated with an increase of blood manganese. Kaohsiung J Med Sci. 1999 May;15(5):297-301.
23. Melo TM, Larsen C, White LR, Aasly J, Sjobakk TE, Flaten TP, Sonnewald U, Syversen T: Manganese, copper, and zinc in cerebrospinal fluid from patients with multiple sclerosis. Biol Trace Elem Res. 2003 Summer;93(1-3):1-8.
24. Lees-Haley PR, Rohling ML, Langhinrichsen-Rohling J: A meta-analysis of the neuropsychological effects of occupational exposure to manganese. Clin Neuropsychol. 2006 Feb;20(1):90-107.
25. Sadek AH, Rauch R, Schulz PE: Parkinsonism due to manganism in a welder. Int J Toxicol. 2003 Sep-Oct;22(5):393-401.
26. Wang X, Li GJ, Zheng W: Upregulation of DMT1 expression in choroidal epithelia of the blood-CSF barrier following manganese exposure in vitro. Brain Res. 2006 Jun 30;1097(1):1-10. Epub 2006 May 26.
27. Takeda A: Manganese action in brain function. Brain Res Brain Res Rev. 2003 Jan;41(1):79-87.
28. Baldwin M, Mergler D, Larribe F, Belanger S, Tardif R, Bilodeau L, Hudnell K: Bioindicator and exposure data for a population based study of manganese. Neurotoxicology. 1999 Apr-Jun;20(2-3):343-53.