Galactosamine

From Wikipedia the free encyclopedia

Galactosamine[1]
Names
IUPAC name
2-Amino-2-deoxy-D-galactose
Other names
α-D-galactosamine
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
UNII
  • InChI=1S/C6H13NO5/c7-3-5(10)4(9)2(1-8)12-6(3)11/h2-6,8-11H,1,7H2/t2-,3-,4+,5-,6?/m1/s1 checkY
    Key: MSWZFWKMSRAUBD-GASJEMHNSA-N checkY
  • InChI=1/C6H13NO5/c7-3-5(10)4(9)2(1-8)12-6(3)11/h2-6,8-11H,1,7H2/t2-,3-,4+,5-,6?/m1/s1
    Key: MSWZFWKMSRAUBD-GASJEMHNBA
  • O[C@H]1[C@@H](O)[C@H](OC(O)[C@@H]1N)CO
Properties
C6H13NO5
Molar mass 179.172 g·mol−1
Melting point 180 °C (356 °F; 453 K) (HCl salt)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Galactosamine is a hexosamine derived from galactose with the molecular formula C6H13NO5. This amino sugar is a constituent of some glycoprotein hormones such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH).

Precursors such as uridine diphosphate (UDP), UDP-N-acetyl-D-glucosamine, or glucosamine are used to synthesize galactosamine in the human body. A derivative of this compound is N-acetyl-D-galactosamine.[2]

Galactosamine is a hepatotoxic, or liver-damaging, agent that is sometimes used in animal models of liver failure.

Hepatotoxicity[edit]

Galactosamine is used to induce hepatitis in rodent liver for research purposes. The result of using galactosamine to induce hepatitis is a disease model in which there is necrosis and inflammation of the liver. This type of tissue damage triggered by galactosamine resembles drug-induced liver disease in humans.[3]

Mechanism of hepatotoxicity[edit]

The proposed mechanism behind galactosamine-induced hepatitis is depletion of the energy source of hepatocytes. In the Leloir pathway galactosamine is metabolized into galactosamine-1-phosphate (by galactokinase) and UDP-galactosamine (by UDP-galactose uridyltransferase). It is hypothesized that this leads to UDP-galactosamine accumulation within cells, and uridine triphosphate (UTP), UDP, and uridine monophosphate (UMP) decrease.[2] The depletion of high-energy molecules such as UTP leads to a disruption in hepatocyte metabolism. Additionally, other derivatives of uridine such as UDP-glucose are depleted and this interferes with glycogen synthesis in the cell.

Another recent hypothesis states that overexpression of pro-inflammatory cytokines (such as tumor necrosis factor (TNFα) and NFκB-dependent inducible nitric oxide synthase (iNOS) over expression play a role in galactosamine-induced damage to liver cells.[3]

See also[edit]

References[edit]

  1. ^ Merck Index, 11th Edition, 4240.
  2. ^ a b Apte, U. (2014), "Galactosamine", Encyclopedia of Toxicology, Elsevier, pp. 689–690, doi:10.1016/b978-0-12-386454-3.00315-8, ISBN 978-0-12-386455-0, retrieved 2022-12-08
  3. ^ a b Das, Joydeep; Ghosh, Jyotirmoy; Roy, Anandita; Sil, Parames C. (April 2012). "Mangiferin exerts hepatoprotective activity against D-galactosamine induced acute toxicity and oxidative/nitrosative stress via Nrf2–NFκB pathways". Toxicology and Applied Pharmacology. 260 (1): 35–47. doi:10.1016/j.taap.2012.01.015. PMID 22310181.

External links[edit]

Retrieved from "https://en.wikipedia.org/w/index.php?title=Galactosamine&oldid=1140869055"