Leukotrien E4
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),() 5353718 (7E,9E,11E,14E),() 44208907 (7E,9E,11Z,14Z),() 53308 (5S,6R),(), 3909 (),() | ||
ChemSpider[3] | 21467210 (5S,7Z,9Z,11E,14Z),() | ||
KEGG[4] | |||
MeSH | |||
ChEBI | 15650 | ||
Jmol-3D slike | Slika 1 | ||
| |||
| |||
Svojstva | |||
Molekulska formula | C23H37NO5S | ||
Molarna masa | 439,61 | ||
| |||
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]
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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
- 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}}