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, T. M.; Kidder, M. S.; Bhattacharyya, N; Xing, W.; Shen, S; Milne GL, Castells MC, Chhay H, Boyce JA (2012). „Cysteinyl leukotriene overproduction in aspirin exacerbated respiratory disease is driven by platelet-adherent leukocytes”. Blood. 119 (16): 3790—8. PMC 3335383 . PMID 22262771. doi:10.1182/blood-2011-10-384826.
^ Lee, C. W.; Lewis, R. A.; Corey EJ; Austen, K. F. (1983). „Conversion of leukotriene D4 to leukotriene E4 by a dipeptidase released from the specific granule of human polymorphonuclear leucocytes”. Immunology. 48: 27—35. PMID 6293969.
^ Sala A, Voelkel N, Maclouf J, Murphy RC (1990). „Leukotriene E4 elimination and metabolism in normal human subjects.”. J Biol Chem (265): 1—8.
^ Lee, T. H.; Christie, P. E. (1993). „Leukotrienes and aspirin induced asthma”. Thorax. 48 (12): 1189—1190. PMC 464963 . PMID 8303620. doi:10.1136/thx.48.12.1189.

Literatura

Lipkowitz, Myron A.; Navarra, Tova (2001). The Encyclopedia of Allergies (2nd изд.). Facts On File. стр. 167. ISBN 0-8160-4404-X. . Facts on File, New York.
Samuelsson, Bengt, ур. (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. Springer. ISBN 1-4020-0146-0. . Kluwer Academic Publishers, Dordrecht,
Bailey, J. Martyn. (1985). Prostaglandins, leukotrienes, and lipoxins: biochemistry, mechanism of action, and clinical applications. Springer. ISBN 0-306-41980-7. . Plenum Press, New York,

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, T. M.; Kidder, M. S.; Bhattacharyya, N; Xing, W.; Shen, S; Milne GL, Castells MC, Chhay H, Boyce JA (2012). „Cysteinyl leukotriene overproduction in aspirin exacerbated respiratory disease is driven by platelet-adherent leukocytes”. Blood. 119 (16): 3790—8. PMC 3335383 . PMID 22262771. doi:10.1182/blood-2011-10-384826.

[5] Lee, C. W.; Lewis, R. A.; Corey EJ; Austen, K. F. (1983). „Conversion of leukotriene D4 to leukotriene E4 by a dipeptidase released from the specific granule of human polymorphonuclear leucocytes”. Immunology. 48: 27—35. PMID 6293969.

[6] Sala A, Voelkel N, Maclouf J, Murphy RC (1990). „Leukotriene E4 elimination and metabolism in normal human subjects.”. J Biol Chem (265): 1—8.

[7] Lee, T. H.; Christie, P. E. (1993). „Leukotrienes and aspirin induced asthma”. Thorax. 48 (12): 1189—1190. PMC 464963 . PMID 8303620. doi:10.1136/thx.48.12.1189.

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