Leukotrien E4

Leukotrien E4
Nazivi
	Preferisani IUPAC naziv Leukotrien E4
	Sistemski IUPAC naziv 6-[(2-amino-2-karboksietil)sulfanil]-5-hidroksikosa-7,9,11,14-tetraenoinska kiselina
Identifikacija
CAS broj	75715-89-8;
3D model (Jmol)	interaktivna slika;
ChEBI	CHEBI:15650;
ChemSpider	21467210 (5S,7Z,9Z,11E,14Z),()?; 21467208 (5S,7Z,9Z,11Z,14Z),()?; 15170118 (7E,9E,11E,14E),()?; 21237688 (5S,6R),(2R)?; 48147 (5S,6R),()?; 3772 (),()?;
KEGG	C05952;
MeSH	Leukotriene+E4
PubChem C ID	5280749 (5S,6R,7E,9E,11Z,14Z),(); 5353718 (7E,9E,11E,14E),(); 44208907 (7E,9E,11Z,14Z),(); 53308 (5S,6R),(); 3909 (),();
	SMILES CCCCCC=CCC=CC=CC=CC(SCC(N)C(O)=O)C(O)CCCC(O)=O; ; ; ; ; ;
Svojstva
Hemijska formula	C23H37NO5S
Molarna masa	439,61
	Ukoliko nije drugačije napomenuto, podaci se odnose na standardno stanje materijala (na 25 °C [77 °F], 100 kPa).
	Reference infokutije

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.^[4] On se formira putem sekvencijalne konverzije od LTC4 do LTD4 i zatim do LTE4, što je krajnji i najstabilniji cisteinilni leukotrien.^[5] 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.^[6] 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.^[7]

Reference

^ 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.
^ 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. PMID 20970519. doi:10.1016/j.drudis.2010.10.003. уреди
^ 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.
^ 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
^ 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
^ Sala A, Voelkel N, Maclouf J, Murphy RC. Leukotriene E4 elimination and metabolism in normal human subjects. J Biol Chem 1990; 265:21771-8
^ 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

Spoljašnje veze

[1] 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.

[2] 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. PMID 20970519. doi:10.1016/j.drudis.2010.10.003. уреди

[3] 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.

[4] 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

[5] 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

[6] Sala A, Voelkel N, Maclouf J, Murphy RC. Leukotriene E4 elimination and metabolism in normal human subjects. J Biol Chem 1990; 265:21771-8

[7] Lee TH, Christie PE. Leukotrienes and aspirin induced asthma. Thorax 1993; 48(12): 1189–1190

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