Leukotrien E4

Leukotrien E4
Naziv po klasifikaciji 6-[(2-amino-2-karboksietil)sulfanil]-5-hidroksikosa-7,9,11,14-tetraenoinska kiselina
Identifikacija
CAS registarski broj 75715-89-8
PubChem[1][2] 5280749 (5S,6R,7E,9E,11Z,14Z),() DaY
5353718 (7E,9E,11E,14E),() DaY
44208907 (7E,9E,11Z,14Z),() DaY
53308 (5S,6R),(), 
3909 (),() DaY
ChemSpider[3] 21467210 (5S,7Z,9Z,11E,14Z),() DaY, 21467208 (5S,7Z,9Z,11Z,14Z),() DaY, 15170118 (7E,9E,11E,14E),() DaY, 21237688 (5S,6R),(2RDaY, 48147 (5S,6R),() DaY, 3772 (),() DaY
KEGG[4] C05952
MeSH Leukotriene+E4
ChEBI 15650
Jmol-3D slike Slika 1
Svojstva
Molekulska formula C23H37NO5S
Molarna masa 439,61



Ukoliko nije drugačije napomenuto, podaci se odnose na standardno stanje (25 °C, 100 kPa) materijala

Infobox references

Leukotrien E4 je cisteinilni leukotrien koji učestvuje u inflamaciji. Poznato je da ga proizvodi nekoliko tipova belih krvnih zrnaca, uključujući eozinofili, mastociti, tkivo makrofaga, i bazofili, i nedavno je utvrđeno da ga proizvode trombociti pričvšćeni za neutrofile.[5] On se formira putem sekvencijalne konverzije od LTC4 do LTD4 i zatim do LTE4, što je krajnji i najstabilniji cisteinilni leukotrien.[6] U poređenju sa kratkim poluživotima LTC4 i LTD4, LTE4 je relativno stabilan i akumulira se u kondenzatu daha, plazmi, i u urinu, što ga čini dominatnim cisteinil leukotrienom u biološkim fluidima.[7] Merenja LTE4, posebno u urinu, se često vrše u kliničkim ispitivanjima.

Povišena produkcija i ekskrecija LTE4 je vezana za nekoliko respiratornih bolesti, i urinarni nivoi LTE4 su povišeni tokom ozbiljnih napada astme, a posebno su visoki kod ljudi sa aspirinom indukovanom astmom.[8]

Reference

  1. Li Q, Cheng T, Wang Y, Bryant SH (2010). „PubChem as a public resource for drug discovery.”. Drug Discov Today 15 (23-24): 1052-7. DOI:10.1016/j.drudis.2010.10.003. PMID 20970519.  edit
  2. Evan E. Bolton, Yanli Wang, Paul A. Thiessen, Stephen H. Bryant (2008). „Chapter 12 PubChem: Integrated Platform of Small Molecules and Biological Activities”. Annual Reports in Computational Chemistry 4: 217-241. DOI:10.1016/S1574-1400(08)00012-1. 
  3. Hettne KM, Williams AJ, van Mulligen EM, Kleinjans J, Tkachenko V, Kors JA. (2010). „Automatic vs. manual curation of a multi-source chemical dictionary: the impact on text mining”. J Cheminform 2 (1): 3. DOI:10.1186/1758-2946-2-3. PMID 20331846.  edit
  4. Joanne Wixon, Douglas Kell (2000). „Website Review: The Kyoto Encyclopedia of Genes and Genomes — KEGG”. Yeast 17 (1): 48–55. DOI:10.1002/(SICI)1097-0061(200004)17:1<48::AID-YEA2>3.0.CO;2-H. 
  5. Laidlaw TM, Kidder MS, Bhattacharyya N, Xing W, Shen S, Milne GL, Castells MC, Chhay H, Boyce JA. Cysteinyl leukotriene overproduction in aspirin exacerbated respiratory disease is driven by platelet-adherent leukocytes. Blood. 2012;119(16):3790-8
  6. Lee CW, Lewis RA, Corey EJ, Austen KF. Conversion of leukotriene D4 to leukotriene E4 by a dipeptidase released from the specific granule of human polymorphonuclear leucocytes. Immunology 1983; 48:27-35
  7. Sala A, Voelkel N, Maclouf J, Murphy RC. Leukotriene E4 elimination and metabolism in normal human subjects. J Biol Chem 1990; 265:21771-8
  8. Lee TH, Christie PE. Leukotrienes and aspirin induced asthma. Thorax 1993; 48(12): 1189–1190

Literatura

  • Lipkowitz, Myron A. and Navarra, Tova (2001) The Encyclopedia of Allergies (2nd ed.) Facts on File, New York, p. 167, ISBN 0-8160-4404-X
  • Samuelsson, Bengt (ed.) (2001) Advances in prostaglandin and leukotriene research: basic science and new clinical applications: 11th International Conference on Advances in Prostaglandin and Leukotriene Research: Basic Science and New Clinical Applications, Florence, Italy, June 4–8, 2000 Kluwer Academic Publishers, Dordrecht, ISBN 1-4020-0146-0
  • Bailey, J. Martyn (1985) Prostaglandins, leukotrienes, and lipoxins: biochemistry, mechanism of action, and clinical applications Plenum Press, New York, ISBN 0-306-41980-7

}{refend}}

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