Salicylhydroxamic acid

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Salicylhydroxamic acid
Salicylhydroxamic acid.png
Names
IUPAC name
2-Hydroxybenzenecarbohydroxamic acid
Identifiers
89-73-6 YesY
ChEBI CHEBI:45615 YesY
ChEMBL ChEMBL309339 YesY
ChemSpider 60011 YesY
Jmol-3D images Image
PubChem 66644
Properties
C7H7NO3
Molar mass 153.14 g·mol−1
Appearance Brownish crystalline powder
Melting point 175 to 178 °C (347 to 352 °F; 448 to 451 K)
Except where noted otherwise, data is given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
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Infobox references

Salicylhydroxamic acid (SHA or SHAM) is a drug that is a potent and irreversible inhibitor of bacterial and plant urease usually used for urinary tract infections. The molecule is similar to urea but is not hydrolyzable by the urease enzyme.[1] It is also a trypanocidal agent. When administered orally, it is metabolized to salicylamide which exerts analgesic, antipyretic and antiinflammatory effects.

Salicylhydroxamic acid is also a common ligand utilized in the synthesis of metallacrowns.

In plants, some fungi and some protists with the alternative oxidase (AOX) enzyme in the mitochondrial electron transport chain system, salicylhdroxamic acid acts as an inhibitor of the enzyme, blocking the largely uninhibited flow of electrons through AOX.[2] AOX acts as a "short circuit" of the normal electron chain, dissipating electrons with a much-decreased translocation of protons, and therefore diminished production of ATP by oxidative phosphorylation. When AOX is blocked by SHAM, electrons are forced through the cytochrome pathway and through cytochrome IV, allowing observation of the operation of the cytochrome pathway without AOX activity. The AOX pathway is found to be the exclusive electron transport pathway in Trypanosoma brucei, the organism that causes African Sleeping Sickness, meaning that SHAM completely shuts down oxygen consumption by this organism.[3][4]

See also[edit]

References[edit]

  1. ^ W. Fishbein and P. Carbone (1965). "Urease Catalysis. II. Inhibition of the Enzyme by Hydroxyurea, Hydroxylamine, and Acetohydroxamic Acid". J Biol Chem 240: 2407–2414. PMID 14304845. 
  2. ^ Anina D. Murphy and Naomi Lang-Unnasch (1999). "Alternative Oxidase Inhibitors Potentiate the Activity of Atovaquone against Plasmodium falciparum". American Society for Microbiology 43 (3): 651–654. PMC 89175. PMID 10049282. 
  3. ^ Minagawa N, Yabu Y, Kita K, Nagai K, Ohta N, Meguro K, Sakajo S, Yoshimoto A (1997). "An antibiotic, ascofuranone, specifically inhibits respiration and in vitro growth of long slender bloodstream forms of Trypanosoma brucei brucei". Mol. Biochem. Parasitol. 84 (2): 271–80. doi:10.1016/S0166-6851(96)02797-1. PMID 9084049. 
  4. ^ Yabu Y, Yoshida A, Suzuki T, Nihei C, Kawai K, Minagawa N, Hosokawa T, Nagai K, Kita K, Ohta N (2003). "The efficacy of ascofuranone in a consecutive treatment on Trypanosoma brucei brucei in mice". Parasitol. Int. 52 (2): 155–64. doi:10.1016/S1383-5769(03)00012-6. PMID 12798927.