By M. Peters-Golden (auth.), Dr Ian Rodger, Dr Jack Botting, Prof. Sven-Erik Dahlén (eds.)
In the 2 many years because the elusive "slow reacting substance of anaphylaxis" (SRS-A) was once pointed out as a fabricated from the motion of the 5-lipoxygenase enzyme on arachidonic acid, it's been good tested that the leukotrienes are key mediators of either alIergy and irritation. Their unencumber through alIergen or different problem has been verified within the lungs of asthmatic topics, and dimension of urinary leukotriene concentrations in such sufferers has been proven to be a worthy, non invasive indicator. major growth has been made in the direction of the characterization of the leukotriene receptor subtypes, exemplified via the cloning of the LTB4 receptor previous this yr. Coupled with this there was a persisted elucidation of sign transduction mechanisms underlying receptor activation. Consequent upon those advances has been the improvement of powerful antagonists of the CysLT receptor, J and either those and inhibitors of leukotriene biosynthesis have entered scientific perform within the treatment of bronchial asthma. during this scientific surroundings antagonists of the CysLTJ receptor were proven to be an efficient treatment in persistent asthmatics, opposed to antigen- and exercise-induced bronchoconstriction, and in aspirin-intolerant asthmatics. the arrival of this new type of brokers gives you to alter the best way asthmatic sufferers are presently treated.
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Additional resources for Leukotrienes: New Concepts and Targets for Therapy
Sample text
It was originally suggested that FLAP would act as a 'docking' protein for 5-LO following its translocation from the cytosol to a membrane site. This would require the formation of a stable complex at the membrane between activated 5-LO, FLAP as well as possibly other components of the LT biosynthetic machinery, such as cytosolic phospholipase A 2 , However, a number of studies has shown a lack of correlation between inhibition of translocation and inhibition of LT biosynthesis 21 - 24 . Current evidence, based in part on the use of a novel photoaffinity analogue of arachidonic ENZYMES INVOLVED IN LEUKOTRIENE 27 SYNTHESIS acid, has suggested that FLAP may act as a fatty acid transfer protein for arachidonic acid facilitating the transfer of arachidonic acid to 5_L025.
Hatzelmann A, Fruchtmann R, Mohrs KH. et al. Mode of action of the leukotriene synthesis (FLAP) inhibitor BAY X 1005. Imphcations for biological regulation of 5-lipoxygenase. Adv Prostaglandin Thrombox Leukot Res. 1994; 22' 23-31. 25. Mancini JA, Abromovitz M, Cox ME, et al. 5-Lipoxygenase-actlvatmg protem is an arachidonate binding protein. FEBS Lett. 1993; 318: 277-81. 26. Hill, E, Maclouf J, Murphy RC, Henson PM. Reversible membrane association of neutrophil 5-lipoxygenase is accompanied by retentIOn of activity and a change m substrate specificity.
Aharony D, Falcone RC. Binding of 3H-LTD. and the peptIde leukotriene antagonist 3H-ICI 198,615 to receptors on human lung membranes. In' Zor U, Naor Z. Danon A, editors Leukotrienes and Prostanoids in Health and Disease. Basel. Karger, 1989: 67-71. 27. Rovati GE, GIOvanazzi S, Mezzetti M, Nicosia S. Heterogeneity of binding sites for 3H-ICI 198,615 in human lung parenchyma. Biochem Pharmacol. 1992; 44: 1411-15. 28. Metters KM, Sawyer N, Nicholson DW. MIcrosomal glutathione S-transferase IS the predominantly leukotriene C.
